Multiple Sclerosis And Parkinson’S Disease Combined

Multiple Sclerosis And Parkinson'S Disease Combined
Multiple Sclerosis And Parkinson'S Disease Combined Image link: https://en.wikipedia.org/wiki/Electroconvulsive_therapy
C O N T E N T S:

KEY TOPICS

  • Movement disorders refer to a group of neurologic disorders that affect the way a person moves, like Parkinson's Disease or Multiple Sclerosis.(More...)
  • Those with MS Are Cautioned About Unsafe Stem Cell Treatments People with multiple sclerosis sometimes become desperate and will travel to other countries for experimental stem cell treatments.(More...)
  • Amy Marriot, PT, talks about movement disorders and how exercise can help patients with Parkinson's Disease improve their quality of life.(More...)
  • Although it is well known that lack of dopamine causes the motor symptoms of Parkinson's disease, it is not clear why the dopamine-producing brain cells deteriorate.(More...)
  • Multiple System Atrophy (MSA): A less common degenerative neurological disorder that causes symptoms similar to Parkinson's disease but with more widespread damage to the central nervous system.(More...)
  • Osmotica, a specialty pharmaceutical company headquartered in Marietta, Georgia with a portfolio and pipeline of Central Nervous System (CNS) drugs to treat multiple sclerosis and Parkinson's, has received the go-ahead for production of Osmolex ER. The drug combines newly patented osmotic technology, that requires only one morning dose a day to provide both immediate and extended release medication.(More...)
  • Unified Parkinson?s Disease Rating Scale (UPDRS): A rating scale used to measure the severity of Parkinson's disease.(More...)
  • Are you trying to regain function of your leg due to Parkinson?s Disease, Stroke, Multiple Sclerosis, or other central nervous system disorders?(More...)

POSSIBLY USEFUL

  • Both diseases can cause your hands to shake, While some signs of MS and Parkinson?s look the same, they?re different diseases.(More...)
  • C. Santangelo, R. Vari, B. Scazzocchio et al., "Anti-inflammatory Activity of Extra Virgin Olive Oil Polyphenols: Which Role in the Prevention and Treatment of Immune-Mediated Inflammatory Diseases?(More...)
  • MS is an autoimmune disease in which the immune system begins to attack healthy tissue in the central nervous system, made up of the brain, spinal cord and optic nerves.(More...)
  • Simpson J, McMillan H, Reeve D. Reformulating psychological difficulties in people with Parkinson’s disease: the potential of a social relational approach to disablism.(More...)
  • Studies of families indicate that relatives of an individual with MS have an increased risk for developing the disease.(More...)

RANKED SELECTED SOURCES

KEY TOPICS

Movement disorders refer to a group of neurologic disorders that affect the way a person moves, like Parkinson's Disease or Multiple Sclerosis. [1] Multiple sclerosis is an inflammatory disease of the nervous system, specifically including nerve cells of the brain and spinal cord. [2] Multiple Sclerosis typically begins in your twenties while Parkinsons disease is for the over 50 crowd. [2] Pediatric Multiple Sclerosis: What You Need to Know Multiple sclerosis (MS) is a progressive disease that typically starts in adulthood. [3]

More people suffer from Parkinson's disease than multiple sclerosis, muscular dystrophy and amyotrophic lateral sclerosis combined. [4] D. S. Pedersen, P. M. Fredericia, M. O. Pedersen et al., "Metallic gold slows disease progression, reduces cell death and induces astrogliosis while simultaneously increasing stem cell responses in an EAE rat model of multiple sclerosis," Histochemistry and Cell Biology, vol. 138, no. 5, pp. 787-802, 2012. [5] S. Saidha, C. Eckstein, and P. A. Calabresi, "New and emerging disease modifying therapies for multiple sclerosis," Annals of the New York Academy of Sciences, vol. 1247, no. 1, pp. 117-137, 2012. [5]

When it comes to caring for neurological disorders such as Parkinson's disease, multiple sclerosis (MS), Guillain-Barré syndrome, balance disorders and Lou Gehrig's disease, our experts know success lies in compassionate, specialized treatment plans. [6] Ding A, Paul F, Dr J. Vitamin D and multiple sclerosis: the role for risk of disease and treatment. [7] Krieger SC, Cook K, De Nino S, Fletcher M. The topographical model of multiple sclerosis: a dynamic visualization of disease course. [7] Kampman MT, Steffensen LH, Mellgren SI, Jgensen L. Effect of vitamin D3 supplementation on relapses, disease progression and measures of function in persons with multiple sclerosis: exploratory outcomes from a double-blind randomised controlled trial. [7] Multiple sclerosis (MS) is a chronic inflammatory demyelination disease of the human CNS that affects young adults and can, over subsequent decades, transform into a progressive neurodegenerative disorder associated with major clinical disabilities. [8] Wood H. Multiple sclerosis: latitude and vitamin D influence disease course in multiple sclerosis. [7] Multiple sclerosis (MS) is defined as a chronic inflammatory disease of the central nervous system (CNS), which results in sclerotic lesions in the brain that gradually lead to motor and sensory deficits. [8] Multiple sclerosis (MS) is the major human demyelinating disease of the central nervous system, affecting most commonly young adults. [8] Prognosis: Americans with multiple sclerosis have a life expectancy seven years shorter than people without the disease. [9] Multiple sclerosis is a long-lasting disease in which the immune system attacks the protective sheath that covers your nerves. [10] To date, statins have been specifically tested and used in atherosclerosis, multiple sclerosis, rheumatoid arthritis, Behcet?s disease, and Kawasaki disease in many cases with very promising results. [11]

In deep brain stimulation, electrodes are placed in the thalamus (to treat essential tremor and multiple sclerosis) or in the globus pallidus (for Parkinson's disease). [12] Diseases that affect the brain, like vascular disease, normal pressure hydrocephalus, multiple sclerosis and Parkinson's disease, can all make it difficult to walk." [13] These tremors are associated with conditions such as Parkinson's disease and multiple sclerosis. [14]

Amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) are both neurodegenerative diseases that affect the central nervous system. [3] Multiple Sclerosis is definitely an autoimmune disease, but in this disease the immune system attacks and destroys myelin, the fatty sheath surrounding nerve fibers. [2]

This study aimed to identify predictors of activity and participation in people with motor neurone disease (MND), people with multiple sclerosis (MS) and people with Parkinson’s Disease (PD). [15] The focus of this study was a comparison of three progressive, neurodegenerative conditions; motor neurone disease (MND), multiple sclerosis (MS) and Parkinson’s disease (PD), where deterioration over time may lead to increased need for services. [15] Kremenchutzky M, Rice GP, Baskerville J, Wingerchuk DM, Ebers GC. The natural history of multiple sclerosis: a geographically based study 9: observations on the progressive phase of the disease. [15] Multiple sclerosis Multiple sclerosis (MS) is a disease where your immune system attacks myelin, the coating that protects the body's nerve cells. [13] Multiple sclerosis is an unpredictable disease, and it affects people in different ways. [14] More Americans are diagnosed with Parkinson?s disease than with multiple sclerosis, muscular dystrophy, and ALS (Lou Gehrig?s disease) combined. [16] Multiple sclerosis is a chronic disease that attacks the central nervous system. [14] Multiple Sclerosis (MS) is the most common disabling neurological disease of young adults. [17] Multiple sclerosis (MS) is a neuroinflammatory disease that affects myelin, a substance that makes up the membrane (called the myelin sheath) that wraps around nerve fibers (axons). [17] Sheep disease toxin shines a light on multiple sclerosis A sheep disease has parallels with multiple sclerosis. [14]

Epidemiological evidence demonstrates that deficiency of Vitamin D is relevant for disease risk and course in multiple sclerosis (MS) and presumably also in neuromyelitis optica spectrum disorders (NMOSD), Parkinson?s disease (PD), and Alzheimer?s disease (AD). [7] M. Srinivasan and D. K. Lahiri, "Significance of NF- ? B as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis," Expert Opinion on Therapeutic Targets, vol. 19, no. 4, pp. 471-487, 2015. [5] Genetic and environmental factors both play a vital role in the progression of neurodegenerative diseases including Parkinson?s disease, Alzheimer?s disease (AD), and multiple sclerosis (MS). [5] Not so long ago, a diagnosis of multiple sclerosis, Parkinson?s disease or lupus meant lifelong disability, chronic pain and even an early death. [9]

Those with MS Are Cautioned About Unsafe Stem Cell Treatments People with multiple sclerosis sometimes become desperate and will travel to other countries for experimental stem cell treatments. [3] How A New Test for Iron in the Brain May Revolutionize MS Treatment A new test that can detect iron levels in different parts of the brain may revolutionize how multiple sclerosis is diagnosed and treated. [3] Multiple sclerosis is a central nervous system disorder that affects the brain and spinal cord. [3] Multiple sclerosis is an inflammatory state of the immune system?it literally passes the blood brain barrier and attacks the myelin sheath that protects neurons. [2] Richard Sater, MD, PhD, discusses the basics of multiple sclerosis and how treatment has changed over time. [1] Multiple Sclerosis, commonly referred to as MS, affects an estimated 2.3 million people worldwide. [1]

K. S. Carbajal, C. Schaumburg, R. Strieter, J. Kane, and T. E. Lane, "Migration of engrafted neural stem cells is mediated by CXCL12 signaling through CXCR4 in a viral model of multiple sclerosis," Proceedings of the National Acadamy of Sciences of the United States of America, vol. 107, no. 24, pp. 11068-11073, 2010. [5] J. G. Weinger, W. C. Plaisted, S. M. Maciejewski, L. L. Lanier, C. M. Walsh, and T. E. Lane, "Activating receptor NKG2D targets RAE-1-expressing allogeneic neural precursor cells in a viral model of multiple sclerosis," Stem Cells, vol. 32, no. 10, pp. 2690-2701, 2014. [5] L. C. M. Arruda, J. T. C. de Azevedo, G. L. V. de Oliveira et al., "Immunological correlates of favorable long-term clinical outcome in multiple sclerosis patients after autologous hematopoietic stem cell transplantation," Clinical Immunology, vol. 169, pp. 47-57, 2016. [5] G. C. Deluca, R. Alterman, J. L. Martin et al., "Casting light on multiple sclerosis heterogeneity: the role of HLA-DRB1 on spinal cord pathology," Brain, vol. 136, no. 4, pp. 1025-1034, 2013. [5] M. L. Greenberg, J. G. Weinger, M. P. Matheu et al., "Two-photon imaging of remyelination of spinal cord axons by engrafted neural precursor cells in a viral model of multiple sclerosis," Proceedings of the National Acadamy of Sciences of the United States of America, vol. 111, no. 22, pp. E2349-E2355, 2014. [5] F. B. S. Briggs, X. Shao, B. A. Goldstein, J. R. Oksenberg, L. F. Barcellos, and P. L. De Jager, "Genome-wide association study of severity in multiple sclerosis," Genes & Immunity, vol. 12, no. 8, pp. 615-625, 2011. [5] K. S. Shindler, E. Ventura, M. Dutt, P. Elliott, D. C. Fitzgerald, and A. Rostami, "Oral resveratrol reduces neuronal damage in a model of multiple sclerosis," Journal of Neuro-Ophthalmology, vol. 30, no. 4, pp. 328-339, 2010. [5] V. K. Harris, Q. J. Yan, T. Vyshkina, S. Sahabi, X. Liu, and S. A. Sadiq, "Clinical and pathological effects of intrathecal injection of mesenchymal stem cell-derived neural progenitors in an experimental model of multiple sclerosis," Journal of the Neurological Sciences, vol. 313, no. 1-2, pp. 167-177, 2012. [5]

Scheel M, Finke C, Oberwahrenbrock T, Freing A, Pech L-M, Schlichting J, et al. Retinal nerve fibre layer thickness correlates with brain white matter damage in multiple sclerosis: a combined optical coherence tomography and diffusion tensor imaging study. [7] Chataway J, Schuerer N, Alsanousi A, Chan D, MacManus D, Hunter K, Anderson V, Bangham CR, Clegg S, Nielsen C, Fox NC, Wilkie D, Nicholas JM, Calder VL, Greenwood J, Frost C, & Nicholas R (2014) Effect of high-dose simvastatin on brain atrophy and disability in secondary progressive multiple sclerosis (MS-STAT): a randomised, placebo-controlled, phase 2 trial. [11] S. V. Abrahamsson, D. F. Angelini, A. N. Dubinsky et al., "Non-myeloablative autologous haematopoietic stem cell transplantation expands regulatory cells and depletes IL-17 producing mucosal-associated invariant T cells in multiple sclerosis," Brain, vol. 136, no. 9, pp. 2888-2903, 2013. [5] R. K. Burt, A. E. Traynor, B. Cohen et al., "T cell-depleted autologous hematopoietic stem cell transplantation for multiple sclerosis: Report on the first three patients," Bone Marrow Transplantation, vol. 21, no. 6, pp. 537-541, 1998. [5] R. K. Burt, R. Balabanov, X. Han et al., "Association of nonmyeloablative hematopoietic stem cell transplantation with neurological disability in patients with relapsing-remitting multiple sclerosis," Journal of the American Medical Association, vol. 313, no. 3, pp. 275-284, 2015. [5]

J. S. Merzaban, J. Imitola, S. C. Starossom et al., "Cell surface glycan engineering of neural stem cells augments neurotropism and improves recovery in a murine model of multiple sclerosis," Glycobiology, vol. 25, no. 12, pp. 1392-1409, 2015. [5] M. J. Kim, J. Y. Lim, S. A. Park et al., "Effective combination of methylprednisolone and interferon ? -secreting mesenchymal stem cells in a model of multiple sclerosis," Journal of Neuroimmunology, vol. 314, pp. 81-88, 2018. [5] S. E. Baranzini, J. Wang, R. A. Gibson et al., "Genome-wide association analysis of susceptibility and clinical phenotype in multiple sclerosis," Human Molecular Genetics, vol. 18, no. 4, pp. 767-778, 2009. [5] Y. Barhum, S. Gai-Castro, M. Bahat-Stromza, R. Barzilay, E. Melamed, and D. Offen, "Intracerebroventricular transplantation of human mesenchymal stem cells induced to secrete neurotrophic factors attenuates clinical symptoms in a mouse model of multiple sclerosis," Journal of Molecular Neuroscience, vol. 41, no. 1, pp. 129-137, 2010. [5] R. E. James, J. Hillis, I. Adorj et al., "Loss of galectin-3 decreases the number of immune cells in the subventricular zone and restores proliferation in a viral model of multiple sclerosis," Glia, vol. 64, no. 1, pp. 105-121, 2016. [5] M. T. Fischer, R. Sharma, J. L. Lim et al., "NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury," Brain, vol. 135, no. 3, pp. 886-899, 2012. [5] D. J. Mahad, I. Ziabreva, G. Campbell et al., "Mitochondrial changes within axons in multiple sclerosis," Brain, vol. 132, no. 5, pp. 1161-1174, 2009. [5] D. Paling, B. S. Solanky, F. Riemer et al., "Sodium accumulation is associated with disability and a progressive course in multiple sclerosis," Brain, vol. 136, no. 7, pp. 2305-2317, 2013. [5] A. S. Fazeli, D. Nasrabadi, A. Pouya et al., "Proteome analysis of post-transplantation recovery mechanisms of an EAE model of multiple sclerosis treated with embryonic stem cell-derived neural precursors," Journal of Proteomics, vol. 94, pp. 437-450, 2013. [5] L. Bai, D. P. Lennon, A. I. Caplan et al., "Hepatocyte growth factor mediates mesenchymal stem cell-induced recovery in multiple sclerosis models," Nature Neuroscience, vol. 15, no. 6, pp. 862-870, 2012. [5] L. Bai, D. P. Lennon, V. Eaton et al., "Human bone marrow-derived mesenchymal stem cells induce Th2-polarized immune response and promote endogenous repair in animal models of multiple sclerosis," Glia, vol. 57, no. 11, pp. 1192-1203, 2009. [5] M. Cobo, P. Anderson, K. Benabdellah et al., "Mesenchymal stem cells expressing vasoactive intestinal peptide ameliorate symptoms in a model of chronic multiple sclerosis," Cell Transplantation, vol. 22, no. 5, pp. 839-854, 2013. [5]

C. Zhang, J. Cao, X. Li et al., "Treatment of multiple sclerosis by transplantation of neural stem cells derived from induced pluripotent stem cells," SCIENCE CHINA Life Sciences, vol. 59, no. 9, pp. 950-957, 2016. [5] M. J. Craner, J. Newcombe, J. A. Black, C. Hartle, M. L. Cuzner, and S. G. Waxman, "Molecular changes in neurons in multiple sclerosis: Altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger," Proceedings of the National Acadamy of Sciences of the United States of America, vol. 101, no. 21, pp. 8168-8173, 2004. [5] S. -G. Guo, C. -J. Wang, G. Zhao, and G. -Y. Li, "Role of Vitamin D in regulating the neural stem cells of mouse model with multiple sclerosis," European Review for Medical and Pharmacological Sciences, vol. 19, no. 21, pp. 4004-4011, 2015. [5] G. La Nasa, R. Littera, E. Cocco, M. G. Marrosu, L. Contu, and L. Battistina, "Allogeneic hematopoietic stem cell transplantation in a patient affected by large granular lymphocyte leukemia and multiple sclerosis," Annals of Hematology, vol. 83, no. 6, pp. 403-405, 2004. [5] M. Cristofanilli, B. Cymring, A. Lu, H. Rosenthal, and S. A. Sadiq, "Cerebrospinal fluid derived from progressive multiple sclerosis patients promotes neuronal and oligodendroglial differentiation of human neural precursor cells in vitro," Neuroscience, vol. 250, pp. 614-621, 2013. [5] D. A. Hafler, A. Compston, S. Sawcer et al., "Risk alleles for multiple sclerosis identified by a genomewide study," The New England Journal of Medicine, vol. 357, no. 9, pp. 851-862, 2007. [5] I. Niki?, D. Merkler, C. Sorbara et al., "A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis," Nature Medicine, vol. 17, no. 4, pp. 495-499, 2011. [5] T. Zeis, A. Probst, A. J. Steck, C. Stadelmann, W. Brk, and N. Schaeren-Wiemers, "Molecular changes in white matter adjacent to an active demyelinating lesion in early multiple sclerosis: molecular changes in MS periplaque white matter," Brain Pathology, vol. 19, no. 3, pp. 459-466, 2009. [5] U. Graumann, R. Reynolds, A. J. Steck, and N. Schaeren-Wiemers, "Molecular changes in normal appearing white matter in multiple sclerosis are characteristic of neuroprotective mechanisms against hypoxic insult," Brain Pathology, vol. 13, no. 4, pp. 554-573, 2003. [5] F. Sato, N. E. Martinez, M. Shahid, J. W. Rose, N. G. Carlson, and I. Tsunoda, "Resveratrol exacerbates both autoimmune and viral models of multiple sclerosis," The American Journal of Pathology, vol. 183, no. 5, pp. 1390-1396, 2013. [5] E. Mikaeili Agah, K. Parivar, and M. T. Joghataei, "Therapeutic effect of transplanted human Wharton's jelly stem cell-derived oligodendrocyte progenitor cells (hWJ-MSC-derived OPCs) in an animal model of multiple sclerosis," Molecular Neurobiology, vol. 49, no. 2, pp. 625-632, 2014. [5] L. Bai, J. Hecker, A. Kerstetter, and R. H. Miller, "Myelin repair and functional recovery mediated by neural cell transplantation in a mouse model of multiple sclerosis," Neuroscience Bulletin, vol. 29, no. 2, pp. 239-250, 2013. [5] S. Haahr, N. Koch-Henriksen, A. Mler-Larsen, L. S. Eriksen, and H. M. Andersen, "Increased risk of multiple sclerosis after late Epstein-Barr virus infection: a historical prospective study.," Multiple Sclerosis (Houndmills, Basingstoke, England), vol. 1, no. 2, pp. 73-77, 1995. [5]

Neurodegenerative diseases such as AD and multiple sclerosis are multifactorial disorders possessing no single particular cause or pathophysiologic mechanism. [5] Multiple sclerosis is an autoimmune disease that develops when the body begins attacking the protective myelin sheaths on nerve cells. [18] Multiple sclerosis (MS) is an autoimmune disease, affects around 2.3 million people worldwide and is the most common neurological disease in young adults. [19] Alzheimer?s disease (AD) and multiple sclerosis are major neurodegenerative diseases, which are characterized by the accumulation of abnormal pathogenic proteins due to oxidative stress, mitochondrial dysfunction, impaired autophagy, and pathogens, leading to neurodegeneration and behavioral deficits. [5] Multiple sclerosis (MS) is an immune-mediated neurodegenerative disease of the central nervous system (CNS), which largely affects young adults with certain genetic backgrounds, often following exposure to several as yet unidentified environmental antigen(s). [8] A. Chaudhuri, "Multiple sclerosis is primarily a neurodegenerative disease," Journal of Neural Transmission, vol. 120, no. 10, pp. 1463-1466, 2013. [5]

J. K. Huang and R. J. M. Franklin, "Regenerative medicine in multiple sclerosis: Identifying pharmacological targets of adult neural stem cell differentiation," Neurochemistry International, vol. 59, no. 3, pp. 329-332, 2011. [5] Y. Wang, J. Imitola, S. Rasmussen, K. C. O'Connor, and S. J. Khoury, "Paradoxical dysregulation of the neural stem cell pathway sonic hedgehog-Gli1 in autoimmune encephalomyelitis and multiple sclerosis," Annals of Neurology, vol. 64, no. 4, pp. 417-427, 2008. [5] S. Rasmussen, J. Imitola, A. Ayuso-Sacido et al., "Reversible neural stem cell niche dysfunction in a model of multiple sclerosis," Annals of Neurology, vol. 69, no. 5, pp. 878-891, 2011. [5]

J. F. Li, D. J. Zhang, T. Geng et al., "The potential of human umbilical cord-derived mesenchymal stem cells as a novel cellular therapy for multiple sclerosis,," Cell Transplantation, vol. 23, supplement 1, pp. S113-S122, 2014. [5] X. Wang, E. A. Kimbrel, K. Ijichi et al., "Human ESC-derived MSCs outperform bone marrow MSCs in the treatment of an EAE model of multiple sclerosis," Stem Cell Reports, vol. 3, no. 1, pp. 115-130, 2014. [5] S. Kyrcz-Krzemie?, G. Helbig, K. Torba, A. Kocl?ga, and M. Krawczyk-Kuli?, "Safety and efficacy of hematopoietic stem cells mobilization in patients with multiple sclerosis," International Journal of Hematology, vol. 21, no. 1, pp. 42-45, 2016. [5]

M. Forte, B. G. Gold, G. Marracci et al., "Erratum: Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis (Proceedings of the National Academy of Sciences of the United States of America (2007) 104, (7558-7563) DOI: 10.1073/pnas.0702228104)," Proceedings of the National Acadamy of Sciences of the United States of America, vol. 104, no. 44, p. 17554, 2007. [5] I. R. Kashani, A. Hedayatpour, P. Pasbakhsh et al., "17 ? -estradiol enhances the efficacy of adipose-derived mesenchymal stem cells on remyelination in mouse model of multiple sclerosis," Acta Medica Iranica, vol. 50, no. 12, pp. 789-797, 2012. [5] J. Qin, A. H. Sikkema, K. van der Bij et al., "GD1a overcomes inhibition of myelination by fibronectin via activation of protein kinase A: Implications for multiple sclerosis," The Journal of Neuroscience, vol. 37, no. 41, pp. 9925-9938, 2017. [5] E. Sundqvist, M. Brnhielm, L. Alfredsson, J. Hillert, T. Olsson, and I. Kockum, "Confirmation of association between multiple sclerosis and CYP27B1," European Journal of Human Genetics, vol. 18, no. 12, pp. 1349-1352, 2010. [5] E. Hoveizi, S. Tavakol, and S. Ebrahimi-Barough, "Neuroprotective Effect of Transplanted Neural Precursors Embedded on PLA/CS Scaffold in an Animal Model of Multiple Sclerosis," Molecular Neurobiology, vol. 51, no. 3, pp. 1334-1342, 2015. [5] S. M. Gold and R. R. Voskuhl, "Estrogen treatment in multiple sclerosis," Journal of the Neurological Sciences, vol. 286, no. 1-2, pp. 99-103, 2009. [5] S. Haahr, A. M. Plesner, B. F. Vestergaard, and P. Hlsberg, "A role of late Epstein-Barr virus infection in multiple sclerosis," Acta Neurologica Scandinavica, vol. 109, no. 4, pp. 270-275, 2004. [5] M. Mohajeri, A. Farazmand, M. Mohyeddin Bonab, B. Nikbin, and A. Minagar, "FOXP3 gene expression in multiple sclerosis patients pre- and post mesenchymal stem cell therapy," Iranian Journal of Allergy, Asthma and Immunology, vol. 10, no. 3, pp. 155-161, 2011. [5] A. Thiruvalluvan, M. Czepiel, Y. A. Kap et al., "Survival and functionality of human induced pluripotent stem cell-derived oligodendrocytes in a nonhuman primate model for multiple sclerosis," Stem Cells Translational Medicine, vol. 5, no. 11, pp. 1550-1561, 2016. [5] M. Ghareghani, K. Zibara, H. Sadeghi et al., "Fluvoxamine stimulates oligodendrogenesis of cultured neural stem cells and attenuates inflammation and demyelination in an animal model of multiple sclerosis," Scientific Reports, vol. 7, no. 1, 2017. [5]

J. Nakahara, M. Maeda, S. Aiso, and N. Suzuki, "Current concepts in multiple sclerosis: autoimmunity versus oligodendrogliopathy," Clinical Reviews in Allergy & Immunology, vol. 42, no. 1, pp. 26-34, 2012. [5] Pierrot-Deseilligny C, Rivaud-Phoux S, Clerson P, de Paz R, Souberbielle J-C. Relationship between 25-OH-D serum level and relapse rate in multiple sclerosis patients before and after vitamin D supplementation. [7] Bhargava P, Cassard S, Steele SU, Azevedo C, Pelletier D, Sugar EA, et al. The vitamin D to ameliorate multiple sclerosis (VIDAMS) trial: study design for a multicenter, randomized, double-blind controlled trial of vitamin D in multiple sclerosis. [7] Dr J, Ohlraun S, Skarabis H, Paul F. Efficacy of Vitamin D Supplementation in Multiple Sclerosis (EVIDIMS Trial): study protocol for a randomized controlled trial. [7]

Simpson S Jr, Taylor B, Blizzard L, Ponsonby A-L, Pittas F, Tremlett H, et al. Higher 25-hydroxyvitamin D is associated with lower relapse risk in multiple sclerosis. [7] Behrens JR, Rasche L, GieRM, Pfuhl C, Wakonig K, Freitag E, et al. Low 25-hydroxyvitamin D, but not the bioavailable fraction of 25-hydroxyvitamin D, is a risk factor for multiple sclerosis. [7] B. D. Trapp and P. K. Stys, "Virtual hypoxia and chronic necrosis of demyelinated axons in multiple sclerosis," The Lancet Neurology, vol. 8, no. 3, pp. 280-291, 2009. [5] R. Dutta and B. D. Trapp, "Relapsing and progressive forms of multiple sclerosis: Insights from pathology," Current Opinion in Neurology, vol. 27, no. 3, pp. 271-278, 2014. [5] N. Pfender, R. Saccardi, and R. Martin, "Autologous hematopoietic stem cell transplantation as a treatment option for aggressive multiple sclerosis," Current Treatment Options in Neurology, vol. 15, no. 3, pp. 270-280, 2013. [5] P. Connick, M. Kolappan, C. Crawley et al., "Autologous mesenchymal stem cells for the treatment of secondary progressive multiple sclerosis: an open-label phase 2a proof-of-concept study," The Lancet Neurology, vol. 11, no. 2, pp. 150-156, 2012. [5] T. Gharibi, M. Ahmadi, N. Seyfizadeh, F. Jadidi-Niaragh, and M. Yousefi, "Immunomodulatory characteristics of mesenchymal stem cells and their role in the treatment of multiple sclerosis," Cellular Immunology, vol. 293, no. 2, pp. 113-121, 2015. [5]

T. Dziedzic, I. Metz, T. Dallenga et al., "Wallerian degeneration: A major component of early axonal pathology in multiple sclerosis," Brain Pathology, vol. 20, no. 5, pp. 976-985, 2010. [5] S. Hametner, I. Wimmer, L. Haider, S. Pfeifenbring, W. Brk, and H. Lassmann, "Iron and neurodegeneration in the multiple sclerosis brain," Annals of Neurology, vol. 74, no. 6, pp. 848-861, 2013. [5] P. Sundstr, P. Juto, G. Wadell et al., "An altered immune response to Epstein-Barr virus in multiple sclerosis: A prospective study," Neurology, vol. 62, no. 12, pp. 2277-2282, 2004. [5] M. Mohajeri, M. Sadeghizadeh, F. Najafi, and M. Javan, "Polymerized nano-curcumin attenuates neurological symptoms in EAE model of multiple sclerosis through down regulation of inflammatory and oxidative processes and enhancing neuroprotection and myelin repair," Neuropharmacology, vol. 99, pp. 156-167, 2015. [5] Y. Blanco, A. Saiz, E. Carreras, and F. Graus, "Changes of matrix metalloproteinase-9 and its tissue inhibitor (TIMP-1) after autologous hematopoietic stem cell transplantation in multiple sclerosis," Journal of Neuroimmunology, vol. 153, no. 1-2, pp. 190-194, 2004. [5] S. Llufriu, M. Sepveda, Y. Blanco et al., "Randomized placebo-controlled phase II trial of autologous mesenchymal stem cells in multiple sclerosis," PLoS ONE, vol. 9, no. 12, Article ID e113936, 2014. [5] G. Shroff, "Evaluation of patients with multiple sclerosis using reverse nutech functional score and expanded disability status scale after human embryonic stem cell therapy," Clinical and Translational Medicine, vol. 5, no. 43, 2016. [5] Soilu-Hninen M, Aivo J, Lindstr B-M, Elovaara I, Sumelahti M-L, FkkilM, et al. A randomised, double blind, placebo controlled trial with vitamin D3 as an add on treatment to interferon ?-1b in patients with multiple sclerosis. [7] Finke C, Schlichting J, Papazoglou S, Scheel M, Freing A, Soemmer C, et al. Altered basal ganglia functional connectivity in multiple sclerosis patients with fatigue. [7] Zhang X, Tao Y, Wang J, Garcia-Mata R, & Markovic-Plese S (2013) Simvastatin inhibits secretion of Th17-polarizing cytokines and antigen presentation by DCs in patients with relapsing remitting multiple sclerosis. [11]

Amy Marriot, PT, talks about movement disorders and how exercise can help patients with Parkinson's Disease improve their quality of life. [1] "Skill acquisition exercises" are another form of exercise that is particularly beneficial to Parkinson's disease patients. [1] Because many Parkinson's disease patients begin to lose the volume of their voice, speech therapy focuses on helping patients talk louder and be better understood. [1]

Alzheimer's disease and primary lateral sclerosis can also be mistaken for Parkinson's disease. [12] What causes multiple sclerosis? Landmark study finds clue Multiple sclerosis is an autoimmune disease, the causes of which remain mysterious. [14]

Shih T, Wakeford C, Meletiche D, Sussell J, Chung A, Liu Y, Shim JJ, & Lakdawalla D (2016) Reconsidering the economic value of multiple sclerosis therapies. [11] Bozkaya D, Livingston T, Migliaccio-Walle K, & Odom T (2017) The cost-effectiveness of disease-modifying therapies for the treatment of relapsing-remitting multiple sclerosis. [11] Mirzaei F, Michels KB, Munger K, O?Reilly E, Chitnis T, Forman MR, et al. Gestational vitamin D and the risk of multiple sclerosis in offspring. [7] Ashtari F, Toghianifar N, Zarkesh-Esfahani SH, Mansourian M. Short-term effect of high-dose vitamin D on the level of interleukin 10 in patients with multiple sclerosis: a randomized, double-blind, placebo-controlled clinical trial. [7] We chose to use a dose of 80?mg of Simvastatin for this study, as this was the dose shown to have an excellent protective effect in the MS STAT trial involving treating Multiple Sclerosis patients. [11]

A. Dulamea, "Mesenchymal stem cells in multiple sclerosis - translation to clinical trials," Journal of Medicine and Life, vol. 8, no. 1, pp. 24-27, 2015. [5] I. Michailidou, H. E. de Vries, E. M. Hol, and M. E. van Strien, "Activation of endogenous neural stem cells for multiple sclerosis therapy," Frontiers in Neuroscience, vol. 9, 2015. [5] A. K. Pandit, K. Prasad, and T. Seth, "Autologous hematopoietic stem cell transplantation in progressive severe multiple sclerosis," Annals of Indian Academy of Neurology, vol. 18, no. 4, pp. 459-463, 2015. [5] Borisow N, Ding A, Pfueller CF, Paul F, Dr J, Hellwig K. Expert recommendations to personalization of medical approaches in treatment of multiple sclerosis: an overview of family planning and pregnancy. [7] Hertwig L, Pache F, Romero-Suarez S, Stner KH, Borisow N, Behrens J, et al. Distinct functionality of neutrophils in multiple sclerosis and neuromyelitis optica. [7] Ciurleo R, Bramanti P, & Marino S (2014) Role of statins in the treatment of multiple sclerosis. [11] Su W, Kansal A, Vicente C, Deniz B, & Sarda S (2016) The cost-effectiveness of delayed-release dimethyl fumarate for the treatment of relapsing-remitting multiple sclerosis in Canada. [11] McDowell T-Y, Amr S, Culpepper WJ, Langenberg P, Royal W, Bever C, et al. Sun exposure, vitamin D intake and progression to disability among veterans with progressive multiple sclerosis. [7] Sotirchos ES, Bhargava P, Eckstein C, Van Haren K, Baynes M, Ntranos A, et al. Safety and immunologic effects of high- vs low-dose cholecalciferol in multiple sclerosis. [7] Dobson R, Giovannoni G, Ramagopalan S. The month of birth effect in multiple sclerosis: systematic review, meta-analysis and effect of latitude. [7] Bakshi R, Yeste A, Patel B, Tauhid S, Tummala S, Rahbari R, et al. Serum lipid antibodies are associated with cerebral tissue damage in multiple sclerosis. [7] Orton S-M, Wald L, Confavreux C, Vukusic S, Krohn JP, Ramagopalan SV, et al. Association of UV radiation with multiple sclerosis prevalence and sex ratio in France. [7] Mahon BD, Gordon SA, Cruz J, Cosman F, Cantorna MT. Cytokine profile in patients with multiple sclerosis following vitamin D supplementation. [7] Correale J, Ysrraelit MC, Gait MI. Immunomodulatory effects of vitamin D in multiple sclerosis. [7] Dr J, Ding A, Paul F. Can we prevent or treat multiple sclerosis by individualised vitamin D supply? EPMA J. 2013;4:4. [7] Nielsen NM, Munger KL, Koch-Henriksen N, Hougaard DM, Magyari M, Jgensen KT, et al. Neonatal vitamin D status and risk of multiple sclerosis: a population-based case-control study. [7] Ascherio A, Munger KL, White R, Khert K, Simon KC, Polman CH, et al. Vitamin D as an early predictor of multiple sclerosis activity and progression. [7] Y. Amir-Levy, K. Mausner-Fainberg, and A. Karni, "Treatment with Anti-EGF Ab Ameliorates Experimental Autoimmune Encephalomyelitis," Multiple Sclerosis International, vol. 2014, Article ID 926134, 9 pages, 2014. [5] Adding to earlier work by Stanislaus et al., Neuhaus et al. using in cells taken from multiple sclerosis patients demonstrated that Simvastatin is more potent as an effective immunomodulatory agent than either Lovastatin and Mevastatin. [11] Taking the example, also conceptually relevant to PD, of the costs of some of the newer multiple sclerosis (patented) therapeutics that are pursuing disease-modification objectives, several of these currently exceed $75,000 per patient per year. [11] Laursen JH, Sdergaard HB, Sensen PS, Sellebjerg F, Oturai AB. Vitamin D supplementation reduces relapse rate in relapsing-remitting multiple sclerosis patients treated with natalizumab. [7] Mowry EM, Waubant E, McCulloch CE, Okuda DT, Evangelista AA, Lincoln RR, et al. Vitamin D status predicts new brain magnetic resonance imaging activity in multiple sclerosis. [7] Munger KL, Zhang SM, O?Reilly E, Hern MA, Olek MJ, Willett WC, et al. Vitamin D intake and incidence of multiple sclerosis. [7] Benjaminsen E, Olavsen J, Karlberg M, Alstadhaug KB. Multiple sclerosis in the far north--incidence and prevalence in Nordland County, Norway, 1970-2010. [7] Farooqi N, Gran B, Constantinescu CS. Are current disease-modifying therapeutics in multiple sclerosis justified on the basis of studies in experimental autoimmune encephalomyelitis? J Neurochem. 2010;115:829-44. [7] Salzer J, Svenningsson A, Sundstr P. Season of birth and multiple sclerosis in Sweden. [7] Kimball SM, Ursell MR, O?Connor P, Vieth R. Safety of vitamin D3 in adults with multiple sclerosis. [7] Munger KL, Levin LI, Hollis BW, Howard NS, Ascherio A. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. [7] Runia TF, Hop WCJ, de Rijke YB, Buljevac D, Hintzen RQ. Lower serum vitamin D levels are associated with a higher relapse risk in multiple sclerosis. [7] Pierrot-Deseilligny C, Souberbielle J-C. Vitamin D and multiple sclerosis: an update. [7] Veauthier C, Paul F. Sleep disorders in multiple sclerosis and their relationship to fatigue. [7] Multiple sclerosis (MS), a chronic inflammatory demyelinating disorder of the central nervous system (CNS), is the most frequent cause of nontraumatic neurological disability among young adults in the Western Hemisphere. [8] Schneider E, Zimmermann H, Oberwahrenbrock T, Kaufhold F, Kadas EM, Petzold A, et al. Optical coherence tomography reveals distinct patterns of retinal damage in neuromyelitis optica and multiple sclerosis. [7] Pfueller CF, Brandt AU, Schubert F, Bock M, Walaszek B, Waiczies H, et al. Metabolic changes in the visual cortex are linked to retinal nerve fiber layer thinning in multiple sclerosis. [7] Spadaro M, Gerdes LA, Krumbholz M, Ertl-Wagner B, Thaler FS, Schuh E, et al. Autoantibodies to MOG in a distinct subgroup of adult multiple sclerosis. [7] Sotgiu S, Pugliatti M, Sotgiu MA, Fois ML, Arru G, Sanna A, et al. Seasonal fluctuation of multiple sclerosis births in Sardinia. [7] Sena A, Pedrosa R, & Morais MG (2007) Beneficial effect of statins in multiple sclerosis: is it dose-dependent? Atherosclerosis, 191, 462. [11] We have long established strong lines of communication between those involved with the multiple sclerosis (MS-STAT) and Simvastatin (PD STAT) trials. [11] Stein MS, Liu Y, Gray OM, Baker JE, Kolbe SC, Ditchfield MR, et al. A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis. [7] Next, we reviewed various stem cell therapies available and how they have proved useful in animal models of AD and multiple sclerosis. [5] Herein, we reviewed the utility of plant polyphenols in regulating proliferation and differentiation of stem cells for inducing brain self-repair in AD and multiple sclerosis. [5] Willer CJ, Dyment DA, Sadovnick AD, Rothwell PM, Murray TJ, Ebers GC. Timing of birth and risk of multiple sclerosis: population based study. [7] Islam T, Gauderman WJ, Cozen W, Mack TM. Childhood sun exposure influences risk of multiple sclerosis in monozygotic twins. [7] Swank RL, Lerstad O, Strom A, Backer J. Multiple sclerosis in rural Norway its geographic and occupational incidence in relation to nutrition. [7] Dr J, Paul F. The transition from first-line to second-line therapy in multiple sclerosis. [7] The results suggest that administering taurine, a molecule naturally produced by human cells, could boost the effectiveness of current multiple sclerosis (MS) therapies. [18] Life expectancy in patients attending multiple sclerosis clinics. [19] New treatments: Ocrevus, shown to slow primary progressive multiple sclerosis and reduce relapses, was approved by the FDA early last year. [9] Cantorna MT, Hayes CE, DeLuca HF. 1,25-Dihydroxyvitamin D3 reversibly blocks the progression of relapsing encephalomyelitis, a model of multiple sclerosis. [7] Mowry EM, Krupp LB, Milazzo M, Chabas D, Strober JB, Belman AL, et al. Vitamin D status is associated with relapse rate in pediatric-onset multiple sclerosis. [7] Dendrou CA, Fugger L, Friese MA. Immunopathology of multiple sclerosis. [7]

Weinshenker B, Bass B, Rice G, Noseworthy J, Carriere W, Baskerville J, Ebers G. The natural history of multiple sclerosis: a geographically based study. [15] Lysandropoulos AP, Havrdova E, ParadigMS Group ‘Hidden’ factors influencing quality of life in patients with multiple sclerosis. [15] Association between use of interferon beta and progression of disability in patients with relapsing-remitting multiple sclerosis. [14] Hyperbaric oxygen therapy, which involves people breathing pure oxygen in a specially designed chamber, for the treatment of multiple sclerosis. (2011, May 29). [14] Braley TJ, Chervin RD. Fatigue in multiple sclerosis: mechanisms, evaluation, and treatment. [15] The term multiple sclerosis refers to the distinctive areas of scar tissue (sclerosis or plaques ) that are visible in the white matter of people who have MS. Plaques can be as small as a pinhead or as large as the size of a golf ball. [17] Omega-3 fatty acids not associated with beneficial effects in multiple sclerosis. [14] Dietary intake of sodium and other minerals and the risk of multiple sclerosis. [14] Multiple sclerosis and extract of cannabis: Results of the MUSEC trial. [14] Multiple sclerosis (MS) is a condition of unknown cause in which the covering lining of nerve fibers (called myelin) is damaged. [20]

Although it is well known that lack of dopamine causes the motor symptoms of Parkinson's disease, it is not clear why the dopamine-producing brain cells deteriorate. [12] Studies have shown that by the time that primary symptoms appear, individuals with Parkinson's disease will have lost 60% to 80% or more of the dopamine-producing cells in the brain. [12] Parkinson's disease is a neurodegenerative disorder, which leads to progressive deterioration of motor function due to loss of dopamine -producing brain cells. [12]

In a 2013 study, Lairson and colleagues showed that the drug benztropine, approved for Parkinson's disease, may also help MS patients by inducing cells called oligodendrocyte precursor cells to mature into myelin-producing oligodendrocytes and repair damaged nerves. [18] In the other forms of parkinsonism, either the cause is known or suspected, or the disorder occurs as a secondary effect of another primary neurological disorder that may have both primary and secondary symptoms of Parkinson's disease. [4] Symptoms of Parkinson's disease vary from patient to patient. [4] Parkinson's disease (PD or, simply, Parkinson's) is the most common form of parkinsonism, a group of motor system disorders. [4] Parkinson's disease is also called primary parkinsonism or idiopathic Parkinson's disease. (Idiopathic is the term for a disorder for which no cause has yet been identified). [4] RWJUH now offers the Gamma Knife, a noninvasive treatment for Parkinson's disease. [4] Parkinson's disease is chronic (persists over a long period of time) and progressive (symptoms grow worse over time). [4] The following are the most common symptoms of Parkinson's disease. [4] The symptoms of Parkinson's disease may resemble other conditions or medical problems. [4]

Discover the symptoms, causes, stages, and treatment options for Parkinson's disease. [12] Deep brain stimulation (or DBS) is a way to inactivate parts of the brain that cause Parkinson's disease and its associated symptoms without purposefully destroying the brain. [12] An estimated 15% of people with Parkinson's symptoms have an Atypical Parkinsonism disorder, which is usually more difficult to treat than Parkinson's disease. [16] Individuals may sometimes be misdiagnosed as having another disorder, and sometimes individuals with Parkinson-like symptoms may be inaccurately diagnosed as having Parkinson's disease. [12] Brain scans and other laboratory tests are also sometimes carried out, mostly to detect other disorders resembling Parkinson's disease. [12] Abnormal clumps called Lewy bodies, which contain the protein alpha-synuclein, are found in many brain cells of individuals with Parkinson's disease. [12] Parkinson's disease and other brain diseases like Parkinson's disease can also cause problems with memory and thinking either at the beginning of the disease or after. [13] Although Parkinson's disease (PD) was first identified in 1817 by Dr. James Parkinson, the cause of PD is still unknown. [16] In most people with Parkinson's disease is idiopathic, which means that it arises sporadically with no known cause. [12] Parkinson's disease Parkinson's disease is a neurological disorder that causes movement problems such as tremors, which usually start in one hand and move throughout the body. [13] Parkinson's disease is the second most common neurodegenerative disorder and the most common movement disorder. [12] Parkinson's disease was named after the British doctor James Parkinson, who in 1817 first described the disorder in detail as "shaking palsy." [12] In earlier stages of Parkinson's disease, substances that mimic the action of dopamine (dopamine agonists), and substances that reduce the breakdown of dopamine (monoamine oxidase type B (MAO-B) inhibitors) can be very efficacious in relieving motor symptoms. [12] In its early stages, Parkinson's disease can resemble a number of other conditions with Parkinson-like symptoms known as Parkinsonism. [12] The severity of Parkinson's disease symptoms and signs vary greatly from person to peson, and it is not possible to predict how quickly the disease will progress. [12] Pahwa, R. and Lyons, K.E. diagnosis of Parkinson's disease: recommendations from diagnostic clinical guidelines. [12] Arenas, E. Towards stem cell replacement therapies for Parkinson's disease. [12] With proper treatment, most individuals with Parkinson's disease can lead long, productive lives. [12] An early and accurate diagnosis of Parkinson's disease is important in developing good treatment strategies to maintain a high quality of life for as long as possible. [12] There is currently no treatment to cure Parkinson's disease. [12] While living with PD can be challenging, there are many things you can do to maintain and improve your quality of life and live well with Parkinson's disease. [21] The most effective therapy for Parkinson's disease is levodopa ( Sinemet ), which is converted to dopamine in the brain. [12] Previous studies of the healthy elderly who exercise, those with Parkinson's disease who exercise, and practitioners of tai chi have found evidence of brain changes by MRI. [20] Most people with Parkinson's disease are diagnosed when they are 60 years old or older, but early-onset Parkinson's disease also occurs. [12] Most people who develop Parkinson's disease are 60 years of age or older. [12] Malnutrition and weight maintenance is often an issue for people with Parkinson's disease. [12] Many people with Parkinson's disease live long productive lives, whereas others become disabled much more quickly. [12] Studies of patent populations with and without Parkinson's Disease suggest the life expectancy for people with the disease is about the same as the general population. [12] Parkinson's disease itself is not a fatal disease, and the average life expectancy is similar to that of people without the disease. [12] Fricker-Gates, R.A. and Gates, M.A. Stem cell-derived dopamine neurons for repair in Parkinson's disease. [12] By studying families with hereditary Parkinson's disease, scientists have identified several genes that are associated with the disorder. [12] Many support groups offer valuable information for individuals with Parkinson's disease and their families on how to cope with the disorder. [12] Age is the largest risk factor for the development and progression of Parkinson's disease. [12] Studying these genes helps understand the cause of Parkinson's disease and may lead to new therapies. [12] Since the exact causes are not known, Parkinson's disease is at present not preventable. [12]

Our physicians specialize in the full range of neurological conditions in children, adolescents, and adults - including stroke, epilepsy, headache, Parkinson's disease, multiple sclerosis, brain and spinal tumors, Alzheimer's disease, and amyotrophic lateral sclerosis (ALS) - and work with a trained team of nurses, social workers, neuropsychologists and others to customize the right treatment plan for you and your family. [22] A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer's disease, stroke, migraine, multiple sclerosis, concussion, Parkinson's disease and epilepsy. [23] Dr. Goodenowe discovered that the inability to make sufficient amounts of plasmalogen molecules to maintain neuronal membrane integrity is the root of the prodrome for several neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. [24] Plasmalogen precursors have been shown to prevent neurodegeneration in models of Parkinson's disease and multiple sclerosis. [24]

Multiple sclerosis (MS) is a disease of the brain and spinal cord where the insulating cells that protect nerves are damaged (a process called demyelination). [24]

This is more than the number of people with multiple sclerosis, muscular dystrophy and Lou Gehrig's Disease combined. [25]

Multiple System Atrophy (MSA): A less common degenerative neurological disorder that causes symptoms similar to Parkinson's disease but with more widespread damage to the central nervous system. [26] RBD is common in people with Parkinson's disease or Multiple System Atrophy. [26]

Publications of Results: Ayan C, Varela S, Vila MH, Seijo-Martinez M, Cancela JM. Treadmill training combined with water and land-based exercise programs: Effects on Parkinson's disease patients. [27] Volpe D, Giantin MG, Maestri R, Frazzitta G. Comparing the effects of hydrotherapy and land-based therapy on balance in patients with Parkinson's disease: a randomized controlled pilot study. [27] Johnson L, Putrino D, James I, Rodrigues J, Stell R, Thickbroom G, Mastaglia FL. The effects of a supervised Pilates training program on balance in Parkinson's disease. [27]

Schmitz-Hbsch T, Pyfer D, Kielwein K, Fimmers R, Klockgether T, Wllner U. Qigong exercise for the symptoms of Parkinson's disease: a randomized, controlled pilot study. [27] Seppi K, Weintraub D, Coelho M, et al. The movement disorder society evidence-based medicine review update: treatments for the non-motor symptoms of Parkinson's disease. [28]

Osmotica, a specialty pharmaceutical company headquartered in Marietta, Georgia with a portfolio and pipeline of Central Nervous System (CNS) drugs to treat multiple sclerosis and Parkinson's, has received the go-ahead for production of Osmolex ER. The drug combines newly patented osmotic technology, that requires only one morning dose a day to provide both immediate and extended release medication. [29] Other neurodegenerative diseases such as multiple sclerosis are more aggressive and occur earlier in life in persons who have the multiple sclerosis prodrome. [24] Guclu-Gunduz A, Citaker S, Irkec C, Nazliel B, Batur-Caglayan HZ. The effects of pilates on balance, mobility and strength in patients with multiple sclerosis. [27] Cattaneo D, Jonsdottir J, Regola A, Carabalona R. Stabilometric assessment of context dependent balance recovery in persons with multiple sclerosis: a randomized controlled study. [27] Anxiety and depression co-occur frequently, and these disorders will affect approximately 50% of patients with PD. 1 Anxiety and depression are more common in persons with PD than in other similarly disabling conditions like diabetes, rheumatoid arthritis, or multiple sclerosis. [28] Kk F, Kara B, Poyraz E, diman E. Improvements in cognition, quality of life, and physical performance with clinical Pilates in multiple sclerosis: a randomized controlled trial. [27] Kalron A, Rosenblum U, Frid L, Achiron A. Pilates exercise training vs. physical therapy for improving walking and balance in people with multiple sclerosis: a randomized controlled trial. [27] The prodrome tests for multiple sclerosis and autism spectrum disorder measure these risk factors. [24] Taurine lends hand to repair cells damaged in multiple sclerosis. [30] Thick axons tend to be through the brain and spinal cord; they are surrounded by a protective fatty sheath called myelin (in multiple sclerosis the myelin is damaged). [26]

Unified Parkinson?s Disease Rating Scale (UPDRS): A rating scale used to measure the severity of Parkinson's disease. [26] Pontone GM, Williams J, Anderson K, et al. Prevalence of anxiety disorders and anxiety subtypes in patients with Parkinson's disease. [28] Mack J, Rabins P, Anderson K, et al. Prevalence of psychotic symptoms in a community-based Parkinson's Disease sample. [28] Pagonabarraga J, Kulisevsky J, Strafella AP, Krack P. Apathy in Parkinson's disease: clinical features, neural substrates, diagnosis, and treatment. [28] Santamato A, Ranieri M, Panza F, Zoccolella S, Frisardi V, Solfrizzi V, Amoruso MT, Amoruso L, Fiore P. Botulinum toxin type A and a rehabilitation program in the treatment of Pisa syndrome in Parkinson's disease. [27] Other Publications: Abbruzzese G, Marchese R, Avanzino L, Pelosin E. Rehabilitation for Parkinson's disease: Current outlook and future challenges. [27] In a 2013 Nature study, Lairson and colleagues showed that the drug benztropine, approved for Parkinson's disease, may also help MS patients by inducing cells called oligodendrocyte precursor cells to mature into myelin-producing oligodendrocytes and repair damaged nerves. [30] Warren N, O'Gorman C, Lehn A, Siskind D. Dopamine dysregulation syndrome in Parkinson's disease: a systematic review of published cases. [28] Ayn C, Cancela JM, Gutirrez-Santiago A, Prieto I. Effects of two different exercise programs on gait parameters in individuals with Parkinson's disease: a pilot study. [27] Parkinson's disease (PD) is a disorder defined and diagnosed by its disabling motor symptoms of bradykinesia, rigidity, and tremor. [28] The FDA announced approval for a new formulation of amantadine, Osmolex ER, which can be used as a treatment for Parkinson's disease (PD). [29] Incidence of Parkinson's disease increases with age, but an estimated four percent of people with PD are diagnosed before age 50. [31] King LA, Salarian A, Mancini M, Priest KC, Nutt J, Serdar A, Wilhelm J, Schlimgen J, Smith M, Horak FB. Exploring outcome measures for exercise intervention in people with Parkinson's disease. [27] Parkinson's disease is a brain and spinal cord disease where patients experience shaking and slow movement, and have difficulty walking. [24] As the neuronal reserve becomes depleted, the symptoms of common neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease begin to appear and then progressively get worse. [24] Because it has many symptoms in common with Alzheimer's and Parkinson's diseases, it can be difficult to diagnose and treat. [23] Hoehn and Yahr scale: A commonly used system for describing how the symptoms of Parkinson's disease progress. [26] Rigidity: A special type of muscle stiffness, which is one of the main symptoms of Parkinson's disease. [26] Di Giulio I, St George RJ, Kalliolia E, Peters AL, Limousin P, Day BL. Maintaining balance against force perturbations: impaired mechanisms unresponsive to levodopa in Parkinson's disease. [27] Dibble LE, Addison O, Papa E. The effects of exercise on balance in persons with Parkinson's disease: a systematic review across the disability spectrum. [27] Wong-Yu IS, Mak MK. Multi-dimensional balance training programme improves balance and gait performance in people with Parkinson's disease: A pragmatic randomized controlled trial with 12-month follow-up. [27] Weiss HD, Adler S. The management of psychosis in Parkinson's disease. [28] Disorders that fall within Parkinson syndrome include Parkinson's disease, atypical Parkinsonism, Parkinson Plus Syndromes, drug-induced Parkinsonism, and normal pressure hydrocephalus. [26] Idiopathic Parkinson's disease: This term is used to describe the common type of Parkinson's disease to distinguish it from other forms of Parkinsonism (also termed "Sporadic PD"). [26] So-called intrinsic factors include underlying cognitive decline, dementia (dementia with Lewy bodies or Parkinson's disease dementia), advanced age, long-standing PD, sleep deprivation, and visual processing abnormalities. [28] FDA Approves Osmotica Pharmaceutical's Once-Daily OSMOLEX ER? (amantadine) extended-release tablets for the treatment of Parkinson's Disease and Drug-Induced Extrapyramidal Reactions in Adults. [29] Mills KA, Greene MC, Dezube R, et al. Efficacy and tolerability of antidepressants in Parkinson's disease: A systematic review and network meta-analysis. [28] Plasmalogen levels are decreased in the brain of persons who suffered with Parkinson's disease prior to death. [24] Parkinson-plus syndromes : A group of neurodegenerative diseases featuring the classical features of Parkinsonism (rigidity, akinesia/ bradykinesia, postural instability and less commonly tremor) with additional features that distinguish them from typical Parkinson's disease. [26]

Are you trying to regain function of your leg due to Parkinson?s Disease, Stroke, Multiple Sclerosis, or other central nervous system disorders? Physical therapy and the Bioness system could help you. [25] Parkinson's disease (PD) is a neurodegenerative disorder that affects predominately dopamine-producing ("dopaminergic") neurons in a specific area of the brain called substantia nigra. [25] The premise of this approach is that stem cells in a dish can be coaxed to become healthy dopamine neurons, which can then be transplanted into the brain to replace the sick and dying neurons in Parkinson's disease. [32] My uncle, Don Anderson, underwent placement of a deep brain stimulation for Parkinson's Disease in 2012. [25] It is unfortunate that not all local doctors (including neurologists) are specialists in Parkinson's disease; thus sometimes a patient's symptoms can be misdiagnosed as Parkinson's. [32] Parkinson's disease is on the increase all over the world, and is now affecting younger people (as young as 30 years of age). [32] This encompasses disorders such as Parkinson's disease (and the Parkinson-Plus disorders such as Shy-Drager Syndrome and Progressive Supranuclear Palsy), essential tremor, dystonia, Restless Leg Syndrome, Myoclonus and Wilson's disease. [32]

POSSIBLY USEFUL

Both diseases can cause your hands to shake, While some signs of MS and Parkinson?s look the same, they?re different diseases. [2] Nerve signals do not traverse the scarred neurons as easily or efficiently as they do through normal nerve cells (think an electrical wire with its insulation stripped off), and this causes the various and unpredictable symptoms of the disease. [2] Developing a treatment plan for MS focuses on slowing down the progression of the disease and managing symptoms. [3] Though both diseases appear to have much in common during the earliest stages, the progression, treatments, and outlook for ALS and MS are very different. [3]

At Cone Health Outpatient Neurorehabilitation Center, therapists work with patients to develop an exercise routine that helps them overcome deficiencies caused by the disease. [1] In both diseases, the symptoms generally start mild, but the symptoms typically progress and worsen over time. [33] By looking for demyelination using an MRI, a doctor can often tell the difference between the two diseases, as signs of demyelination often occur well after symptoms have progressed in ALS. Finally, there?s no single definitive test to distinguish between the two, but signs, symptoms, and imaging are often used to come to a conclusion. [3] There is no cure for MS, but there are many medications available that manage symptoms and slow the progression of the disease. [1] To diagnosis MS, your physician will take an MRI of your brain and spinal cord to look for signs of the disease. [1] Pain syndromes, in general, are common with MS and occur in approximately 55 percent of people with the disease. [33] In both conditions, it is not common for younger people to get the disease, but it is possible. [33] In 2014, almost 16,000 U.S. people were reported to be living with ALS. The Centers for Disease Control and Prevention (CDC) estimates that about 5,000 people are diagnosed with ALS every year. [3] It?s been estimated that up to 50 percent of people with ALS may experience some mild to moderate cognitive or behavioral changes due to ALS. As the disease progresses, some people have gone on to develop dementia. [3]

The disease can cause the nerves themselves to deteriorate or become permanently damaged. [1] MS can be treated and "tamed" parkinsons can be treated but both diseases are known to be progressive if discovered too late. [2]

Parkinson?s Disease is characterized by the death of brain cells which produce a neurotransmitter called dopamine. [2] This can create lesions in your brain that cause Parkinson?s disease. [34] I was worried that my dad had Parkinson?s at one point, thankfully after spending hours on Youtube I came across this video which helps to detect early signs of Parkinson?s disease. [2] You?ll notice that there are some similarities - and differences - in MS and Parkinson?s disease. [33] Unfortunately, yes - it is possible to have co-existing MS and Parkinson?s disease. [33] A typical Parkinson?s disease might start as a tremor, continue to having difficulty moving feet to walk (called fessening feet), and on to both cognitive and physical issues. [2]

In its wake, it leaves plaques, or scars (thus the name "multiple sclerosis" meaning "many scars"). [2] Before starting an exercise program, it's important to talk with a physical therapist who specializes in patients with Parkinson's so they can individualize the exercises to the needs of the patient. [1]

C. Santangelo, R. Vari, B. Scazzocchio et al., "Anti-inflammatory Activity of Extra Virgin Olive Oil Polyphenols: Which Role in the Prevention and Treatment of Immune-Mediated Inflammatory Diseases? Endocrine, metabolic & immune disorders drug targets," Endocrine, Metabolic & Immune Disorders - Drug Targets, vol. 18, pp. 36-50, 2018. [5] D. Valenti, L. de Bari, D. de Rasmo et al., "The polyphenols resveratrol and epigallocatechin-3-gallate restore the severe impairment of mitochondria in hippocampal progenitor cells from a Down syndrome mouse model," Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, vol. 1862, no. 6, pp. 1093-1104, 2016. [5] V. Vukic, D. Callaghan, D. Walker et al., "Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer's brain is mediated by the JNK-AP1 signaling pathway," Neurobiology of Disease, vol. 34, no. 1, pp. 95-106, 2009. [5] D. C. Rubinsztein, M. DiFiglia, N. Heintz et al., "Autophagy and its possible roles in nervous system diseases, damage and repair.," Autophagy, vol. 1, no. 1, pp. 11-22, 2005. [5]

E. J. Gong, H. R. Park, M. E. Kim et al., "Morin attenuates tau hyperphosphorylation by inhibiting GSK3 ?," Neurobiology of Disease, vol. 44, no. 2, pp. 223-230, 2011. [5] E. Vasileiou, R. M. Montero, C. M. Turner, and G. Vergoulas, "P2X7 receptor at the heart of disease," Hippokratia, vol. 14, no. 3, pp. 155-163, 2010. [5]

Jarius S, Ruprecht K, Wildemann B, Kuempfel T, Ringelstein M, Geis C, et al. Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: a multicentre study of 175 patients. [7] K. B. Pandey and S. I. Rizvi, "Plant polyphenols as dietary antioxidants in human health and disease," Oxidative Medicine and Cellular Longevity, vol. 2, no. 5, pp. 270-278, 2009. [5] Disease G. B. D., Injury I., Prevalence C., "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015", Lancet, vol. 388, pp. 1545-1602, 2016. [5] R. Khera and N. Das, "Complement Receptor 1: Disease associations and therapeutic implications," Molecular Immunology, vol. 46, no. 5, pp. 761-772, 2009. [5]

The International PD Linked Clinical Trial committee is tasked to analyze potential new target therapies for PD and for which the biochemical evidence indicates the likelihood that they may have benefit to slow, halt or reverse disease progression in patients with PD. This large global committee of PD experts, many of whom have extensive experience in PD trials and their design, is coordinated by The Cure Parkinson?s Trust. [11] Shan Y, Tan S, Zhang L, Huang J, Sun X, Wang Y, et al. Serum 25-hydroxyvitamin D3 is associated with disease status in patients with neuromyelitis optica spectrum disorders in south China. [7] A "real-world" study investigating the association between serum vitamin D levels on disease course in patients with disease-modifying drugs of MS such as interferon-?, glatiramer acetate and fingolimod found differences in the effect of serum vitamin D levels on the relapse rate and gadolinium-enhancing lesions in the different treatment classes. [7] Serum vitamin D levels of 75 nmol/l (30 ng/ml) are safe and may potentially exert therapeutic effects in some patients with neurodegenerative and neuroinflammatory diseases such as reduced disability worsening, improved bone health, and improved cognition. [7] Animal models of PD have been often used to test the efficacy of vitamin D in the disease pathology in terms of dopamine production, neurotrophic factors synthesis, as well as the possible neuroprotective effect of vitamin D. In a rat model of PD, intraperitoneal injection of 1,25(OH)2D3 before or after inducing PD partially restored tyrosine hydroxylase expression in the substantia nigra thus promoting the conversion of tyrosine to dopamine. [7]

Wu DC, Teismann P, Tieu K, Vila M, Jackson-Lewis V, Ischiropoulos H, & Przedborski S (2003) NADPH oxidase mediates oxidative stressin the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model ofParkinson?s disease. [11] Suda K, Tahara N, Honda A, Yoshimoto H, Kishimoto S, Kudo Y, Kaida H, Abe T, Ueno T, & Fukumoto Y (2015) Statin reduces persistent coronary arterial inflammation evaluated by serial 1 8fluorodeoxyglucose positron emission tomography imaging long after Kawasaki disease. [11] Cho HY, Kim K, Kim YB, Kim H, & No JH (2017) Expression patternsof Nrf2 and Keap1 in ovarian cancer cells and their prognosticrole in disease recurrence and patient survival. [11]

It was pointed out in the review by Roy & Pahan that effector T cells may exacerbate disease progression (which can be demonstrated in post mortem PD brains), while regulatory T cells (Tregs) tend to occupy a protective role. [11] Pathophysiologically, autoreactive encephalitogenic T cells in concert with B cells and cells of the innate immune system orchestrate an autoimmune reaction against CNS structures which results in demyelination and neuroaxonal damage of the brain, retina, and spinal cord from earliest disease stages on. [7] F. Aboul-Enein, H. Rauschka, B. Kornek et al., "Preferential loss of myelin-associated glycoprotein reflects hypoxia-like white matter damage in stroke and inflammatory brain diseases," Journal of Neuropathology & Experimental Neurology, vol. 62, no. 1, pp. 25-33, 2003. [5]

Ding A, Pfueller CF, Paul F, Dr J. Exercise in multiple sclerosis--an integral component of disease management. [7] Brundin P, Barker RA, Conn PJ, Dawson TM, Kieburtz K, Lees AJ, Schwarzschild MA, Tanner CM, Isaacs T, Duffen J, Matthews H, & Wyse RK (2013) Linked clinical trials-the development of new clinical learning studies in Parkinson?s disease using screening of multiple prospective new treatments. [11] Tison F, Nre-Pag L, Meissner WG, Dupouy S, Li Q, Thiolat ML, Thiollier T, Galitzky M, Ory-Magne F, Milhet A, Marquine L, Spampinato U, Rascol O, & Bezard E (2013) Simvastatin decreases levodopa-induced dyskinesia in monkeys, but not in a randomized, placebo-controlled, multiple cross-over ("n-of-1") exploratory trial of simvastatin against levodopa-induced dyskinesia in Parkinson?s disease patients. [11] Two randomized, double-blind and placebo-controlled studies using 20,000 IU cholecalciferol per week also failed to detect significant effects on clinical parameters of disease activity although one study showed significantly fewer gadolinium-enhancing lesions on brain MRI. [7]

Kendrick J, Targher G, Smits G, Chonchol M. 25-Hydroxyvitamin D deficiency is independently associated with cardiovascular disease in the Third National Health and Nutrition Examination Survey. [7] Tousoulis D, Psarros C, Demosthenous M, Patel R, Antoniades C, & Stefanadis C (2014) Innate and adaptive inflammation as a therapeutic target in vascular disease: the emerging role of statins. [11]

Prognosis: People with Parkinson?s who do not exhibit dementia have only a one-year lower life expectancy than those who do not have the disease. [9] Bosco DA, Fowler DM, Zhang Q, Nieva J, Powers ET, Wentworth P Jr, Lerner RA, & Kelly JW (2006) Elevated levels of oxidized cholesterol metabolites in Lewy body disease brains accelerate alpha-synuclein fibrilization. [11] Mealy MA, Newsome S, Greenberg BM, Wingerchuk D, Calabresi P, Levy M. Low serum vitamin D levels and recurrent inflammatory spinal cord disease. [7] Martin HL, Santoro M, Mustafa S, Riedel G, Forrester JV, & &Teismann P (2016) Evidence for a role of adaptive immune responsein the disease pathogenesis of the MPTP mouse model of Parkinson?sdisease. [11]

Min J-H, Waters P, Vincent A, Cho H-J, Joo B-E, Woo S-Y, et al. Low levels of vitamin D in neuromyelitis optica spectrum disorder: association with disease disability. [7] Vitamin D levels were significantly lower in patients who had monophasic spinal cord inflammation compared to recurrent disease, and vitamin D insufficiency (< 30 ng/ml) was associated with a fourfold (CI 1.60-10.0) increased risk of recurrence, along with other predictors of recurrent disease. [7] In sum, despite inconclusive results from the few studies above, it is in light of the devastating disease course of many NMOSD patients and the significantly increased risk of recurrence following a first episode of myelitis in case of vitamin D insufficiency advisable to measure vitamin D levels in patients with NMOSD and to raise these to above 30 ng/ml (75 nmol/l). [7] In the next section, we discuss the (1) geographical and seasonal associations of vitamin D with the risk and course of MS, (2) associations between vitamin D supply or serum levels in early years and the risk to develop MS later, (3) relations between serum levels and clinical and/or radiographical disease activity, and finally, (4) data from interventional clinical trials. [7] Starting vitamin D treatment at the onset of symptoms (therapeutic paradigm) ameliorated the course and severity of the disease. [7] We here review the possible role of vitamin D in the pathogenesis and disease course of MS, NMOSD, PD, and AD and potential therapeutic effects of vitamin D supplementation which may be relevant for predictive, preventive, and personalized medicine. [7] There are very few interventional studies that have been undertaken to investigate a potentially beneficial effect of vitamin D on the disease course in PD. The human studies have focused on the polymorphisms of vitamin D receptors. [7] The pre-treatment with vitamin D depicted positive effect in triggering NSCs, thereby preventing the development and progression of disease and also hindering apoptosis in a mice model of MS. [5] The studies presented in this review suggest that whether vitamin D may have beneficial effects in disease course or not, may be dependent on factors such as ethnicity, gender, diet, vitamin D receptor (VDR) polymorphisms and sunlight exposure. [7] The few interventional trials undertaken so far to investigate whether vitamin D supplementation can beneficially influence the disease course have been methodologically fairly heterogeneous, and study designs have not always been appropriate. [7] In all these diseases, it is reported that patients tend to have low serum vitamin D levels compared to healthy controls. [7] Patients that received vitamin D supplements had better disease rating compared to the placebo group. [7]

It is projected that if PD disease progression could be slowed by just 20% it would overall save approximately $76,000 per patient, rising to a saving of approximately $440,000 per patient if PD progression could be stopped altogether. [11] Simvastatin as a Neuroprotective Treatment for ModerateParkinson?s Disease (PD STAT) https://clinicaltrials.gov/ct2/show/NCT02787590 Last verified April 2017. [11] In 2014 Abdanipour et al., studying PGC-1? and Nrf2 expression on cell survival and apoptosis demonstrated that Lovastatin protects bone marrow stromal cell-derived neural stem cells against oxidative stress-induced cell death, and suggested it as a candidate for the treatment of neurological diseases that involve oxidative stress. [11] A retrospective study involving a cohort of 419 PD patients, showed that in PD patients who received either a statin or a fibrate, their mean age of disease onset was delayed by nearly 9 years when compared with PD patients who were not taking any lipid-lowering treatment. [11] In a study, intraventricularly injected Olig2-NSCs significantly reduced the clinical signs of acute and relapsing disease, thereby ameliorating CREAE in mice MS model. [5] Bioliberation of gold ions from metallic gold implants in an EAE rodent model of MS showed reduced apoptotic cell death, upregulation of neuroprotective proteins Metallothionein-1 and -2 in the corpus callosum, significant upregulation of NSCs migrating from the SVZ, and significant slowing of disease progression. [5] Removing the dysfunctional immune cells that cause the autoimmune condition can halt the disease, though replacing the entire immune system is a risky procedure. [19]

Although the disease may appear in younger patients (even teenagers), it usually affects people in late middle age. [4] Worldwide, about 24 million people suffer from the disease, and this number is expected to double by 2040.The neuropathology of the disease is characterized by neurofibrillary tangles and senile plaques in the brain. [7] A 2015 study on the global prevalence of MS reported 2.3 million people affected by the disease. [5] In 2016, the U.S. Preventative Services Task Force advised the use of statins for people between 40 and 75 years old who carry at least one risk factor for heart disease, and who have more than a 10% risk of heart disease. [11] Most would agree that the hypothetical risk of a healthy individual acquiring PD through taking a particular medication, represents a very different scenario to using that same medication to treat the disease once it has already developed. [11] Several studies have found that sunlight exposure attenuates disease course in many diseases such as MS and PD among others due to its influence on circulating vitamin D levels. [7] Dietary treatment of mice with vitamin D starting from disease induction (prophylactic paradigm) resulted in a reduced incidence and severity of the disease. [7] Other treatments include medications that may slow the course of the disease, ease symptoms, prevent or treat attacks or help manage the stress that can come with MS. [10] The clinical course of RRMS is characterized by clear disease relapses with development of new neurologic deficits or worsening of older symptoms that last more than 24 hours; each relapse is typically separated from the last attack by at least 1 month of stability. [8] The intrathecally transplanted iPSC derived NPCs after disease onset-ameliorated clinical and pathological features of EAE by exerting a neuroprotective effect through the secretion of LIF that promotes survival, differentiation, and remyelination capacity of both endogenous oligodendrocyte precursors and mature oligodendrocytes, thereby possessing therapeutic potential against MS. [5] Duan C, Du ZD, Wang Y, & Jia LQ (2014) Effect of pravastatin on endothelial dysfunction in children with medium to giant coronary aneurysms due to Kawasaki disease. [11] Partly because of this confounding inter-relationship, there is currently no clarity about whether statin use is protective of an individual developing PD, has no effect, or makes it more likely that an individual may develop the disease. [11] Although the exact mechanism underlying vitamin D effects in these diseases remains widely unexplored, human and animal studies continue to provide some hints. [7] Although tempting, these studies are limited by the inevitably biased retrospective determination of past sun exposure and the possibility of intrinsic vitamin D independent effects of sun or UVB exposure itself on the disease. [7] Several interventional studies investigating the effect of vitamin D on disease severity either by supplementation with vitamin D as add-on therapy or UVB phototherapy are ongoing. [7] Most studies assessing the effect of vitamin D on cognition have focused on the elderly populations with chronic neurological diseases and concomitant low vitamin D levels. [7] This throws more emphasis on whether vitamin D levels decrease with age and as to whether prolonged low levels of vitamin D are associated with the incidence of diseases in the adulthood thus highlighting the need to investigate the effect of reverse causation more thoroughly. [7]

Both genetic and environmental factors contribute to the individual risk of MS. Several lines of evidence which are discussed in more detail below suggest vitamin D as an environmental factor to impact both the risk to develop MS as well as the course of the already established disease. [7]

L. G. Apostolova, "Alzheimer disease," Continuum: Lifelong Learning in Neurology, vol. 22, no. 2, pp. 419-434, 2016. [5] Ahuja M, Ammal Kaidery N, Yang L, Calingasan N, Smirnova N, Gaisin A, Gaisina IN, Gazaryan I, Hushpulian DM, Kaddour-Djebbar I, Bollag WB, Morgan JC, Ratan RR, Starkov AA, Beal MF, & Thomas B (2016) Distinct Nrf2 signaling mechanisms of fumaric acid esters and their role in neuroprotection against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced experimental Parkinson?s-like disease. [11]

Sykiotis GP, & Bohmann D (2010) Stress-activated cap?n?collar transcription factors in aging and human disease. [11] In this review, we discuss the understanding of pathophysiology of AD and MS. Further we discuss how stem cells have proved their efficacy against these two diseases and finally how polyphenols can target stem cells for inducing brain self-repair or neurogenesis process (generation of new neurons) in AD and MS. 1.1. [5] Lastly, we discussed how polyphenols utilize the potential of stem cells, either complementing their therapeutic effects or stimulating endogenous and exogenous neurogenesis, against these diseases. [5] Their conclusion was that lipid-lowering drugs may have a disease modifying effect. [11]

There is an ongoing scientific debate as to whether adult patients with MOG antibodies should be diagnosed with NMOSD or whether MOG-antibody associated encephalomyelitis is a disease entity in its own. [7] One in five patients will experience this form of the disease for at least 20 years ( benign MS ) but most will eventually convert to a phase of gradual functional decline. [8] The disease in these patients is called secondary progressive phase MS (SP-MS). [8] Approximately 6% of patients with PP-MS also experience relapses in parallel with their disease progression and are said to have progressive-relapsing MS (PR-MS). [8] In 50% to 80% of patients with RR disease, progressive deterioration with less marked attacks occurs within 10 years of onset. [8] We elected to recruit patients in mid-stage disease, H&Y <or ??3 in the ON state, but who had developed motor fluctuations. [11] Autologous HSCs transplantation has been shown to completely halt disease activity in the majority of patients with aggressive MS. [5] In EAE mice, adult NG2 + cells represent a valuable cell population for initiation of neural repair in demyelinating diseases such as MS. [5] While the cause of the disease remains elusive, it is primarily thought to be an autoimmune disorder. [5] Although the exact causes remain elusive, genetic and environmental factors contribute to the disease risk. [7] The UK National Institute for Health and Clinical Excellence has endorsed the use of statins in those with an estimated 10% risk of developing cardiovascular disease over the next decade. [11] "Cardiovascular disease: Risk assessment and reduction, including lipid modification at www.nice.org.uk ". [11]

Accordingly, increasing annual healthcare costs per PD patient are associated with more advanced stages of the disease, with greater burden resulting from cognitive decline, increased non-motor symptoms and development of balance impairment and falls. [11] The disease is characterized by episodes of neurologic symptoms occurring over a period of days to weeks, followed by complete or incomplete remissions of various durations. [8] Intraperitoneal administration of MSCs expressing vasoactive intestinal peptide (VIP) stopped progression and reduced symptoms in EAE when administered at the peak of disease. [5] Extra virgin olive oil and its polyphenols have been shown to improve MS disease symptoms. [5]

What it is: A disease in which the immune system attacks the central nervous system, destroying myelin, the substance that protects nerves in the brain, spinal cord and optic nerve. [9] Hallmarks of these diseases are impairment of Ubiquitin Proteasome Pathway and accumulation of pathogenic proteins in the discrete brain regions due to oxidative and nitrosative stress, mitochondrial dysfunction, and impaired autophagy. [5]

This has enabled early disease detection and treatment initiation. [8] By directly inhibiting key inflammatory processes, Simvastatin may therefore represent a therapeutically beneficial disease modifying agent with considerable potential to reduce the rate of PD progression. [11] The flavonoid-enriched fraction AF4 in mouse EAE MS model demonstrated disease recovery from EAE and reduced neuropathology in the cerebellum and spinal cord. [5] MS is the most common neurological disease in young adults, with about 400,000 people in the U.S. and more than 2 million people globally having the disease. [10] U.S. Preventive Services Task Force, Bibbins-Domingo K, Grossman DC, Curry SJ, Davidson KW, Epling JW Jr, Garc'a FA, Gillman MW, Kemper AR, Krist AH, Kurth AE, Landefeld CS, LeFevre ML, Mangione CM, Phillips WR, Owens DK, Phipps MG, & Pignone MP (2016) Statin use for the primary prevention of cardiovascular disease in adults: U.S. Preventive Services Task Force Recommendation Statement. [11] Withdrawal of vitamin D leads to a resumption of disease activity. [7] Data consistently show a clear association between higher vitamin D levels with a less active disease course. [7] Prevalence of vitamin D insufficiency and deficiency (< 30 ng/ml or 75 nmol/l) ranged from 73 to 80%, without a difference between groups and no association with disease activity and neurological disability. [7] Two earlier studies had investigated the association between vitamin D levels and inflammatory spinal cord disease, a subgroup of which had a final diagnosis of NMOSD. [7] Whether higher serum levels and/or a personalized high-dose vitamin D supplementation are superior in the prevention or modification of individual disease courses remains to be clarified. [7]

In this study, the Hoehn and Yahr scale and the UPDRS were used to assess disease severity. [7] With a relatively small sample size and a clinically heterogeneous condition, it is important to allow sufficient time for measurable disease progression across the study population. [11]

Huang X, Auinger P, Eberly S, Oakes D, Schwarzschild M, Ascherio A, Mailman R, Chen H ; Parkinson Study Group DATATOP Investigators (2011) Serum cholesterol and the progression of Parkinson?s disease: results from DATATOP. PLoS One, 6, e22854. [11] M. L. Selley, D. R. Close, and S. E. Stern, "The effect of increased concentrations of homocysteine on the concentration of (E)-4-hydroxy-2-nonenal in the plasma and cerebrospinal fluid of patients with Alzheimer's disease," Neurobiology of Aging, vol. 23, no. 3, pp. 383-388, 2002. [5] S. Oddo, A. Caccamo, J. D. Shepherd et al., "Triple-transgenic model of Alzheimer's Disease with plaques and tangles: intracellular A ? and synaptic dysfunction," Neuron, vol. 39, no. 3, pp. 409-421, 2003. [5] J. E. Young, J. Boulanger-Weill, D. A. Williams et al., "Elucidating molecular phenotypes caused by the SORL1 Alzheimer's disease genetic risk factor using human induced pluripotent stem cells," Cell Stem Cell, vol. 16, no. 4, pp. 373-385, 2015. [5] D. H. Kim, D. Lee, E. H. Chang et al., "GDF-15 secreted from human umbilical cord blood mesenchymal stem cells delivered through the cerebrospinal fluid promotes hippocampal neurogenesis and synaptic activity in an Alzheimer's disease model," Stem Cells and Development, vol. 24, no. 20, pp. 2378-2390, 2015. [5] L. K. Hamilton, M. Dufresne, S. E. Joppet al., "Aberrant lipid metabolism in the forebrain niche suppresses adult neural stem cell proliferation in an animal model of Alzheimer?s disease," Cell Stem Cell, vol. 17, no. 4, pp. 397-411, 2015. [5]

M. K. Wetzel-Smith, J. Hunkapiller, T. R. Bhangale et al., "A rare mutation in UNC5C predisposes to late-onset Alzheimer's disease and increases neuronal cell death," Nature Medicine, vol. 20, no. 12, pp. 1452-1457, 2014. [5] Reynolds AD, Banerjee R, Liu J, Gendelman HE, & Mosley RL (2007) Neuroprotective activities of CD4+CD25+ regulatory T cells in an animal model of Parkinson?s disease. [11] Rozani V, Giladi N, El-Ad B, Gurevich T, Tsamir J, Hemo B, & Peretz C (2017) Statin adherence and the risk of Parkinson?s disease: A population-based cohort study. [11] Swallow DM, Lawton MA, Grosset KA, Malek N, Klein J, Baig F, Ruffmann C, Bajaj NP, Barker RA, Ben-Shlomo Y, Burn DJ, Foltynie T, Morris HR, Williams N, Wood NW, Hu MT, & Grosset DG (2016) Statins are underused in recent-onset Parkinson?s disease with increased vascular risk: findings from the UK Tracking Parkinson?s and Oxford Parkinson?s Disease Centre (OPDC) discovery cohorts. [11]

Bai S, Song Y, Huang X, Peng L, Jia J, Liu Y, & Lu H (2016) Statin use and the risk of Parkinson?s disease: An updated meta-analysis. [11] Bar-On P, Crews L, Koob AO, Mizuno H, Adame A, Spencer B, & Masliah E (2008) Statins reduce neuronal alpha-synuclein aggregation in in vitro models of Parkinson?s disease. [11] Liu G, Sterling NW, Kong L, Lewis MM, Mailman RB, Chen H, Leslie D, & Huang X (2017) Statins may facilitate Parkinson?s disease: Insight gained from a large, national claims database. [11] Undela K, Gudala K, Malla S, & Bansal D (2013) Statin use and risk of Parkinson?s disease: a meta-analysis of observational studies. [11] Eriksson I, Nath S, Bornefall P, Giraldo AM, &. llinger K (2017) Impact of high cholesterol in a Parkinson?s disease model: Prevention of lysosomal leakage versus stimulation of ?-synuclein aggregation. [11] Ghosh A, Roy A, Matras J, Brahmachari S, Gendelman HE, & Pahan K (2009) Simvastatin inhibits the activation of p21ras and prevents the loss of dopaminergic neurons in a mouse model of Parkinson?s disease. [11]

MS is an autoimmune disease in which the immune system begins to attack healthy tissue in the central nervous system, made up of the brain, spinal cord and optic nerves. [1] ALS isn?t an autoimmune disease, but a nervous system disorder. [3]

Simpson J, McMillan H, Reeve D. Reformulating psychological difficulties in people with Parkinson’s disease: the potential of a social relational approach to disablism. [15] A recent study looks at exercise as a potential treatment for people with relapsing-remitting MS. What's different, and exciting, about this study is that it not only analyzed the impact of exercise on symptoms of the disease, it also assessed how the brain changed with exercise treatment. [20] Balestrino R, Martinez-Martin P. Neuropsychiatric symptoms, behavioural disorders, and quality of life in Parkinson’s disease. [15] Considering non-dopaminergic dysfunction in motor symptoms, tremor is defined as involuntary, rhythmic and alternating movements of one or more body parts; resting tremor is "typical" in PD and present in about 75% of patients with the disease. 26 Importantly, tremor-dominant patients follow a more benign course. [35] Maffoni M, Giardini A, Pierobon A, Ferrazzoli D, Frazzitta G. Stigma Experienced by Parkinson’s disease patients: a descriptive review of qualitative studies. [15] Prevalence : A measurement of all individuals affected by the disease at a particular time (for example, the number of people with Parkinson?s on March 19, 2018). [21] By supporting this study, the Foundation works to better understand Parkinson?s with the goal of solving this disease. [21]

Regression analyses identified multiple predictors of activity and participation dependent on Ox-PAQ domain and disease group, the most prominent being social and physical functioning as measured by the MOS SF-36. [15] Some of people diagnosed with Parkinson's also have family members with the disease. [12] PARK2 (Parkinson's disease autosomal recessive, juvenile 2): The PARK2 gene makes the protein parkin. [12]

Amyotrophic lateral sclerosis (ALS, Lou Gehrig's disease) is a neurological disease that progresses rapidly. [12] Therefore, this drug should be used as a last resort to treat patients with a form of MS that leads to rapid loss of function and for whom other treatments did not stop the disease. [17] For some patients, symptoms are so mild that they do not notice anything until later in the course of the disease. [14] There is still no cure for MS, but there are treatments for initial attacks, medications and therapies to improve symptoms, and recently developed drugs to slow the worsening of the disease. [17] These are relevant aspects since non-dopaminergic features have significant impact on the course of PD and correlate with disease duration ( Figure 1 ). 24 These include issues such as sleep problems, cognitive impairment, depression, autonomic disturbances and psychic symptoms. [35] Currently available animal models share many of the same disease mechanisms and symptoms as MS, but they do not fully mimic the disease. [17]

"Vascular disease in the brain can cause people to walk slowly and cautiously," said Dr. Finney, director of the Geisinger Memory and Cognition Program. [13] Alzheimer's is a condition that affects your memory and ability to think, but vascular disease can cause changes in many different tasks the brain performs, especially walking. [13] MS may cause depression as part of the disease process, since it damages myelin and nerve fibers inside the brain. [17]

Gibbons CJ, Thornton EW, Ealing J, Shaw PJ, Talbot K, Tennant A, Young CA, UKMND-QoL Group Assessing social isolation in motor neurone disease: a rasch analysis of the MND social withdrawal scale. [15] Whilst MND, MS and PD sit under the broad umbrella of neurological disease, their clinical characteristics are markedly different. [15] Other studies are trying to find ways to stop progression of the disease in MS patients with primary progressive MS or secondary progressive MS, and to restore neurological function in these individuals. [17] Each patient should have a scheduled follow-up evaluation by his or her neurologist 6 to 12 months after the initial diagnostic evaluation, even in the absence of any new attacks of the disease. [17]

People of Northern European descent appear to be at the highest risk for the disease, regardless of where they live. [17] People with MS, especially those who have had the disease for a long time, can experience difficulty with thinking, learning, memory, and judgment. [17] Until recently, it appeared that a minority of people with MS had very mild disease or "benign MS" and would never get worse or become disabled. [17] People with MS may experience several types of pain during the course of the disease. [17] People who experience this are described as having "relapsing-remitting" disease. [20] The life expectancy is about the same as people without the disease. [12] Many people, myself included, believe that the usefulness of non-medication approaches for chronic disease may be underrecognized. [20]

This allows them to look for proteins and inflammatory cells associated with the disease and to rule out other diseases that may look similar to MS, including some infections and other illnesses. [17] The disease attacks the nerve cells responsible for the control of voluntary muscles. [12]

There is debate among doctors about whether to start disease modulating drugs at the first signs of MS or to wait until the course of the disease is better defined before beginning treatment. [17] It has been noted that the main factors leading to the development of dyskinesia include denervation of the dopaminergic system, disease duration and severity, dopaminergic treatment and pulsatile stimulation of post-synaptic DA receptors. 77,78 Dyskinesia can also initiate when levodopa levels are stable. [35] "These treatments don't slow down the progression of the disease, but they do help ease the symptoms." [13]

A diagnosis of MS is often delayed because MS shares symptoms with other neurological conditions and diseases. [17] They all agree the disease is a progressive disease with symptoms that usually occur in one stage may overlap or occur in another stage. [12] The best chance of reversing the problems with walking, incontinence, and thinking is if normal pressure hydrocephalus is caught within 6 months of the first symptom, there is a chance for improvement or halting the disease. [13]

Having a more accurate animal model would reduce the time and expense of testing therapies that may not prove to be successful in treating the human disease. [17] Huntington's disease is the result of degeneration of neurons in areas of the brain. [12] Vascular disease is caused by damage to the blood vessels in the brain from issues like high blood pressure, high cholesterol, high blood sugar and smoking. [13]

While Alzheimer's can't be stopped, vascular disease can be, so it is important to find it and treat it as early as possible. [13] Gomperts SN, Rentz DM, Moran E, et al. Imaging amyloid deposition in Lewy body diseases. [35] They can be very helpful in the initial diagnosis, to rule out other disorders, as well as in monitoring the progression of the disease to make therapeutic adjustments. [12]

MS is considered the most common chronic inflammatory disorder of the CNS in western countries and -- as it is an incurable disease -- a leading course of disability and early retirement in young adults, predominantly females of child-bearing age. [7] Zamvil SS, Slavin AJ. Does MOG Ig-positive AQP4-seronegative opticospinal inflammatory disease justify a diagnosis of NMO spectrum disorder? Neurol Neuroimmunol Neuroinflamm. 2015;2:e62. [7] The role of polyphenols against other diseases such as disorders of the metabolism can be tested in case of neurodegeneration. [5]

Therapies include anti-symptomatic drugs, monoclonal antibodies, stem cell therapy, and disease management. [5] Although the causes of AD remain unknown, environmental and genetic factors have been suggested to be associated with the disease. [7] It is speculated that the accumulation of A? induces inflammatory responses which account for the neurodegenerative component of the disease resulting in cognitive decline. [7] Based on the clinical disease pattern, four types of MS are recognized: relapsing-remitting MS (RRMS), secondary progressive MS (SPMS), primary progressive MS (PPMS), and progressive relapsing MS (PRMS). [8] Clinical manifestations are varied, and can involve any functional neurological system depending on the affected area of the CNS. Diagnostic definitions of MS have undergone significant changes over the last decade, and now rely on both clinical and radiographic criteria of disease dissemination in time and space with improved diagnostic sensitivity and specificity. [8]

Therefore there is a compelling need, shared by patients, families and healthcare systems alike, to identify a cost-effective approach to intercept disease progression, to slow, stop or even reverse neurodegeneration in a rapidly expanding global population of PD patients. [11]

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CC is the chief investigator of PD STAT, a clinical trial exploring Simvastatin as a neuroprotective treatment for patients with Parkinson?s disease. [11] The Simvastatin trial is a 198 patient, 23 Centre, Phase II, randomized, placebo-controlled, double-blinded study, officially titled " Simvastatin as a Neuroprotective Treatment for Parkinson?s Disease: a Double-blind, Randomised, Placebo Controlled Futility Study in Patients of Moderate Severity?. [11]

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They argued that chronic inflammation offers a clear biochemical mechanism which can promote the development of PD. Huang et al. recently showed in multiple models that Simvastatin ameliorated memory deficits in patients with Alzheimer?s disease as well as in laboratory models of AD, and that it achieved this through reduction of mRNA expression of inflammatory cytokines and mediators as well as by improving neuronal survival, supporting earlier work by Wang et al. [11] Based on recommendations of an international committee of experts who are currently bringing multiple, potentially disease-modifying, PD therapeutics into long-term neuroprotective PD trials, a clinical trial involving 198 patients is underway to determine whether Simvastatin provides protection against chronic neurodegeneration. [11] Several laboratory studies have demonstrated multiple biochemical neuroprotective effects of statins in models of PD; these will be reviewed and discussed below. [11]

Evidence from cross-sectional studies has shown the impact of vitamin D deficiency on falls and balance in Parkinson?s disease (PD). [7] Sato Y, Kikuyama M, Oizumi K. High prevalence of vitamin D deficiency and reduced bone mass in Parkinson?s disease. [7] Mosley RL, Benner EJ, Kadiu I, Thomas M, Boska MD, Hasan K, Laurie C, & Gendelman HE (2006) Neuroinflammation, oxidative stress and the pathogenesis of Parkinson?s disease. [11]

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Dunnett SB, Bjklund A. Prospects for new restorative and neuroprotective treatments in Parkinson?s disease. [7] Studies from North America and China investigating the role of vitamin D levels in PD patients found an association between plasma and serum vitamin D levels and disease severity (measured by the Hoehn and Yahr stage and the Unified Parkinson?s Disease Rating Scale (UPDRS)). [7] Kowal SL, Dall TM, Chakrabarti R, Storm MV, & Jain A (2013) The current and projected economic burden of Parkinson?s disease in the United States. [11] Paul R, Choudhury A, & Borah A (2015) Cholesterol - A putative endogenous contributor towards Parkinson?s disease. [11] Kumaran R, & Cookson MR (2015) Pathways to Parkinsonism Redux: convergent pathobiological mechanisms in genetics of Parkinson?s disease. [11]

Johnson SJ, Diener MD, Kaltenboeck A, Birnbaum HG, & Siderowf AD (2013) An economic model of Parkinson?s disease: Implications for slowing progression in the United States. [11] Kang SY, Lee SB, Kim HJ, Kim HT, Yang HO, & Jang W (2017) Autophagic modulation by rosuvastatin prevents rotenone-induced neurotoxicity in an in vitro model of Parkinson?s disease. [11] Castro AA, Wiemes BP, Matheus FC, Lapa FR, Viola GG, Santos AR, Tasca CI, & Prediger RD (2013) Atorvastatin improves cognitive, emotional and motor impairments induced by intranasal 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration in rats, an experimental model of Parkinson?s disease. [11] Study of Urate Elevation in Parkinson?s Disease, Phase 3(SURE-PD3) https://clinicaltrials.gov/show/NCT02642393 Verified June 28 2017. [11] Wolozin B, Wang SW, Li NC, Lee A, Lee TA, & Kazis LE (2007) Simvastatin is associated with a reduced incidence of dementia and Parkinson?s disease. [11] Ascherio A, & Schwarzschild MA (2016) The epidemiology of Parkinson?s disease: Risk factors and prevention. [11] Sheng Z, Jia X, & Kang M (2016) Statin use and risk of Parkinson?s disease: A meta-analysis. [11] Mandel SA, Morelli M, Halperin I, Korczyn AD. Biomarkers for prediction and targeted prevention of Alzheimer?s and Parkinson?s diseases: evaluation of drug clinical efficacy. [7] Van Den Eeden SK, Tanner CM, Bernstein AL, Fross RD, Leimpeter A, Bloch DA, et al. Incidence of Parkinson?s disease: variation by age, gender, and race/ethnicity. [7] Beal MF (1998) Excitotoxicity and nitric oxide in Parkinson?s disease pathogenesis. [11] Hutter-Saunders JA, Mosley RL, & Gendelman HE (2011) Pathways towards an effective immunotherapy for Parkinson?s disease. [11] Kannarkat GT, Boss JM, & Tansey MG (2013) The role of innate andadaptive immunity in Parkinson?s disease. [11]

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We here review the possible role of vitamin D in the pathogenesis and disease course of MS, NMOSD, PD, and AD and potential therapeutic effects of vitamin D supplementation which may be relevant for predictive and/or personalized medicine and may inform individualized treatment strategies for patients with these often debilitating neuroinflammatory and neurodegenerative diseases. [7] ?aczma?ski ?, Jakubik M, Bednarek-Tupikowska G, Rymaszewska J, S?oka N, Lwow F. Vitamin D receptor gene polymorphisms in Alzheimer?s disease patients. [7] Mizwicki MT, Menegaz D, Zhang J, Barrientos-Dur A, Tse S, Cashman JR, et al. Genomic and nongenomic signaling induced by 1?,25(OH)2-vitamin D3 promotes the recovery of amyloid-? phagocytosis by Alzheimer?s disease macrophages. [7] Afzal S, Bojesen SE, Nordestgaard BG. Reduced 25-hydroxyvitamin D and risk of Alzheimer?s disease and vascular dementia. [7] Hoang T, Choi DK, Nagai M, Wu DC, Nagata T, Prou D, Wilson GL, Vila M, Jackson-Lewis V, Dawson VL, Dawson TM, Chesselet MF, & Przedborski S (2009) Neuronal NOS and cyclooxygenase-2 contribute to DNA damage in a mouse model of Parkinson disease. [11] Clarke CE, Patel S, Ives N, Rick CE, Dowling F, Woolley R, et al. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial. [7] Dorsey ER, Constantinescu R, Thompson JP, Biglan KM, Holloway RG, Kieburtz K, Marshall FJ, Ravina BM, Schifitto G, Siderowf A, & Tanner CM (2007) Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030. [11]

Studies of families indicate that relatives of an individual with MS have an increased risk for developing the disease. [17] There are some rare and unusual variants of MS. One of these is Marburg variant MS (also called malignant MS), which causes a swift and relentless decline resulting in significant disability or even death shortly after disease onset. [17] Longer-term studies are needed before we know whether improvements associated with exercise are actually due to exercise, reflect the pattern of the disease, or have some other cause. [20]

MS is confirmed when positive signs of the disease are found in different parts of the nervous system at more than one time interval and there is no alternative diagnosis. [17]

Seppi K, Weintraub D, Coelho M, et al. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson?s disease. [35] Fox SH, Katzenschlager R, Lim SY, et al. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the motor symptoms of Parkinson?s disease. [35]

Devos D, Defebvre L, Bordet R. Dopaminergic and non-dopaminergic pharmacological hypotheses for gait disorders in Parkinson?s disease. [35] Momin S, Mahlknecht P, Georgiev D, et al. Impact of subthalamic deep brain stimulation frequency on upper limb motor function in Parkinson?s disease. [35] Wirdefeldt K, Odin P, Nyholm D. Levodopa-carbidopa intestinal gel in patients with Parkinson?s disease: a systematic review. [35] Trenkwalder C, Chaudhuri KR, Martinez-Martin P, et al. Prolonged-release oxycodone-naloxone for treatment of severe pain in patients with Parkinson?s disease (PANDA): a double-blind, randomised, placebo-controlled trial. [35] Cattaneo C, Barone P, Bonizzoni E, Sardina M. Effects of safinamide on pain in fluctuating Parkinson?s disease patients: a post-hoc analysis. [35] Elmer LW, Surmann E, Boroojerdi B, Jankovic J. Long-term safety and tolerability of rotigotine transdermal system in patients with early-stage idiopathic Parkinson?s disease: a prospective, open-label extension study. [35] Kassubek J, Chaudhuri KR, Zesiewicz T, et al. Rotigotine transdermal system and evaluation of pain in patients with Parkinson?s disease: a post hoc analysis of the RECOVER study. [35] Rios Romenets S, Anang J, Fereshtehnejad SM, et al. Tango for treatment of motor and non-motor manifestations in Parkinson?s disease: a randomized control study. [35] Ikeda K, Yoshikawa S, Kurokawa T, et al. TRK-820, a selective kappa opioid receptor agonist, could effectively ameliorate L-DOPA-induced dyskinesia symptoms in a rat model of Parkinson?s disease. [35] In considering dopaminergic treatment of Parkinson?s disease (PD), one must consider dopaminergic drug targets, effect sizes of dopaminergic approaches, management of motor and non-motor complications, 1 impact of non-motor symptoms and lastly the role of non-dopaminergic mechanisms. [35] Goetz CG, Damier P, Hicking C, et al. Sarizotan as a treatment for dyskinesias in Parkinson?s disease: a double-blind placebo-controlled trial. [35] Borgohain R, Szasz J, Stanzione P, et al. Randomized trial of safinamide add-on to levodopa in Parkinson?s disease with motor fluctuations. [35] Svenningsson P, Rosenblad C, Af Edholm Arvidsson K, et al. Eltoprazine counteracts L-DOPA-induced dyskinesias in Parkinson?s disease: a dose-finding study. [35] Politis M, Wu K, Loane C, et al. Serotonergic mechanisms responsible for levodopa-induced dyskinesias in Parkinson?s disease patients. [35] Muller T, Hoffmann JA, Dimpfel W, Oehlwein C. Switch from selegiline to rasagiline is beneficial in patients with Parkinson?s disease. [35] Cattaneo C, Muller T, Bonizzoni E, et al. Long-term effects of safinamide on mood fluctuations in Parkinson?s disease. [35] Fidalgo C, Ko WK, Tronci E, et al. Effect of serotonin transporter blockade on L-DOPA-induced dyskinesia in animal models of Parkinson?s disease. [35] Cattaneo C, Ferla RL, Bonizzoni E, Sardina M. Long-term effects of safinamide on dyskinesia in mid- to late-stage Parkinson?s disease: a post-hoc analysis. [35]

Rosengren L, Brogardh C, Jacobsson L, Lexell J. Life satisfaction and associated factors in persons with mild to moderate Parkinson?s disease. [35] Minguez-Minguez S, Solis-Garcia Del Pozo J, Jordan J. Rasagiline in Parkinson?s disease: a review based on meta-analysis of clinical data. [35] Robakis D, Fahn S. Defining the role of the monoamine oxidase-B inhibitors for Parkinson?s disease. [35] Qamhawi Z, Towey D, Shah B, et al. Clinical correlates of raphe serotonergic dysfunction in early Parkinson?s disease. [35] Calabresi P, Picconi B, Parnetti L, Di Filippo M. A convergent model for cognitive dysfunctions in Parkinson?s disease: the critical dopamine-acetylcholine synaptic balance. [35]

Do you know how it works? The causes? The symptoms? Take the Parkinson?s Disease Quiz to Test your knowledge of Parkinson's. [12] Li BD, Cui JJ, Song J, et al. Comparison of the efficacy of different drugs on non-motor symptoms of Parkinson?s disease: a network meta-analysis. [35] Liu J, Dong J, Wang L, et al. Comparative efficacy and acceptability of antidepressants in Parkinson?s disease: a network meta-analysis. [35] Negre-Pages L, Regragui W, Bouhassira D, et al. Chronic pain in Parkinson?s disease: the cross-sectional French DoPaMiP survey. [35] Talati R, Reinhart K, Baker W, et al. Pharmacologic treatment of advanced Parkinson?s disease: a meta-analysis of COMT inhibitors and MAO-B inhibitors. [35] Stowe R, Ives N, Clarke CE, et al. Meta-analysis of the comparative efficacy and safety of adjuvant treatment to levodopa in later Parkinson?s disease. [35] Bezard E, Carta M. Could the serotonin theory give rise to a treatment for levodopa-induced dyskinesia in Parkinson?s disease? Brain. 2015;138:829-30. [35] Gjerloff T, Fedorova T, Knudsen K, et al. Imaging acetylcholinesterase density in peripheral organs in Parkinson?s disease with 11C-donepezil PET. Brain. 2015;138:653-63. [35]

Cilia R, Siri C, Canesi M, et al. Dopamine dysregulation syndrome in Parkinson?s disease: from clinical and neuropsychological characterisation to management and long-term outcome. [35] Rascol O, Fitzer-Attas CJ, Hauser R, et al. A double-blind, delayed-start trial of rasagiline in Parkinson?s disease (the ADAGIO study): prespecified and post-hoc analyses of the need for additional therapies, changes in UPDRS scores, and non-motor outcomes. [35] Pahwa R, Tanner CM, Hauser RA, et al. Amantadine extended release for levodopa-induced dyskinesia in Parkinson?s disease (EASED Study). [35] Katzenschlager R, Manson AJ, Evans A, et al. Low dose quetiapine for drug induced dyskinesias in Parkinson?s disease: a double blind cross over study. [35] LeWitt PA, Pahwa R, Sedkov A, et al. Pulmonary safety and tolerability of inhaled levodopa (CVT-301) administered to patients with Parkinson?s disease. [35] Rascol O, Brooks DJ, Korczyn AD, et al. A five-year study of the incidence of dyskinesia in patients with early Parkinson?s disease who were treated with ropinirole or levodopa. [35] Mak E, Su L, Williams GB, et al. Baseline and longitudinal grey matter changes in newly diagnosed Parkinson?s disease: ICICLE-PD study. [35] Valkovic P, Minar M, Singliarova H, et al. Pain in parkinson?s disease: a cross-sectional study of its prevalence, types, and relationship to depression and quality of life. [35] Rosqvist K, Hagell P, Odin P, et al. Factors associated with life satisfaction in Parkinson?s disease. [35]

Brefel-Courbon C, Grolleau S, Thalamas C, et al. Comparison of chronic analgesic drugs prevalence in Parkinson?s disease, other chronic diseases and the general population. [35] Tison F, Keywood C, Wakefield M, et al. A phase 2A trial of the novel mGluR5-negative allosteric modulator dipraglurant for levodopa-induced dyskinesia in Parkinson?s disease. [35] Alam M, Rumpel R, Jin X, et al. Altered somatosensory cortex neuronal activity in a rat model of Parkinson?s disease and levodopa-induced dyskinesias. [35] Bohnen NI, Kaufer DI, Hendrickson R, et al. Cortical cholinergic denervation is associated with depressive symptoms in Parkinson?s disease and parkinsonian dementia. [35]

Zhao Q, Cai D, Bai Y. Selegiline rescues gait deficits and the loss of dopaminergic neurons in a subacute MPTP mouse model of Parkinson?s disease. [35] Incidence of Parkinson?s disease increases with age, but an estimated four percent of people with PD are diagnosed before age 50. [21] When a large population of people have a disease like Parkinson?s disease (PD), it?s essential to have accurate numbers of how many people have the disease, where they live and why they have it. [21]

Parkinson?s disease is an incurable neurodegenerative disorder that causes tremor of the hands, arms, legs, jaw and face; rigidity of the limbs and trunk; slowness of movement; and impaired balance and coordination. [16] Parkinson?s disease is the second most common neurodegenerative disorder after Alzheimer?s disease. [16] Szeto JY, Lewis SJ. Current treatment options for Alzheimer?s disease and Parkinson?s disease dementia. [35] Fox SH. Non-dopaminergic treatments for motor control in Parkinson?s disease. [35] Freitas ME, Fox SH. Nondopaminergic treatments for Parkinson?s disease: current and future prospects. [35]

Iderberg H, McCreary AC, Varney MA, et al. Activity of serotonin 5-HT(1A) receptor "biased agonists? in rat models of Parkinson?s disease and L-DOPA-induced dyskinesia. [35] Wictorin K, Widner H. Memantine and reduced time with dyskinesia in Parkinson?s Disease. [35] Broen MP, Braaksma MM, Patijn J, Weber WE. Prevalence of pain in Parkinson?s disease: a systematic review using the modified QUADAS tool. [35] From recent evidence-based reviews, the most efficacious drugs include levodopa, dopamine agonists (pergolide, piribedil, ropinirole, pramipexole, rotigotine) and monoamine oxidase B (MAO-B) inhibitors (selegiline, rasagiline). 2-7 Among these, following levodopa, pergolide is considered to have the largest effect size, followed by pramipexole (measured by Unified Parkinson?s Disease Rating Scale total score versus placebo). [35] Santini E, Valjent E, Fisone G. Parkinson?s disease: levodopa-induced dyskinesia and signal transduction. [35] Johnston TH, Versi E, Howson PA, et al. DPI-289, a novel mixed delta opioid agonist / mu opioid antagonist (DAMA), has L-DOPA-sparing potential in Parkinson?s disease. [35]

Progression of Parkinson?s disease and unmet needs in mid- to late-stage patients. [35] Blair HA, Dhillon S. Safinamide: a review in Parkinson?s disease. [35] Stowe RL, Ives NJ, Clarke C, et al. Dopamine agonist therapy in early Parkinson?s disease. [35] Gandolfi M, Geroin C, Antonini A, et al. Understanding and treating pain syndromes in Parkinson?s disease. [35] Dafsari HS, Silverdale M, Strack M, et al. Nonmotor symptoms evolution during 24 months of bilateral subthalamic stimulation in Parkinson?s disease. [35] During the pan-European event, world-renowned experts in Parkinson?s disease (PD) presented the latest findings in the pathophysiology and management of the disease. [35] Talati R, Baker WL, Patel AA, et al. Adding a dopamine agonist to preexisting levodopa therapy vs. levodopa therapy alone in advanced Parkinson?s disease: a meta analysis. [35] The entire published study is available in the Parkinson?s Foundation scientific journal, npj Parkinson?s Disease. [21] Firbank MJ, Yarnall AJ, Lawson RA, et al. Cerebral glucose metabolism and cognition in newly diagnosed Parkinson?s disease: ICICLE-PD study. [35] Sommerauer M, Fedorova TD, Hansen AK, et al. Evaluation of the noradrenergic system in Parkinson?s disease: an 11C-MeNER PET and neuromelanin MRI study. [35] Huot P, Johnston TH, Koprich JB, et al. The pharmacology of L-DOPA-induced dyskinesia in Parkinson?s disease. [35] Huot P, Sgambato-Faure V, Fox SH, McCreary AC. Serotonergic approaches in Parkinson?s disease: translational perspectives, an update. [35] Fox SH, Metman LV, Nutt JG, et al. Trial of dextromethorphan/quinidine to treat levodopa-induced dyskinesia in Parkinson?s disease. [35] LeWitt PA, Hauser RA, Grosset DG, et al. A randomized trial of inhaled levodopa (CVT-301) for motor fluctuations in Parkinson?s disease. [35] Bjornestad A, Forsaa EB, Pedersen KF, et al. Risk and course of motor complications in a population-based incident Parkinson?s disease cohort. [35] Some may have a continuous trembling of the head, limbs, and body, especially during movement, although such trembling is more common with other disorders such as Parkinson?s disease. [17] Kim HJ, Jeon B. How close are we to individualized medicine for Parkinson?s disease? Expert Rev Neurother. 2016;16:815-30. [35] Schrag A, Quinn N. Dyskinesias and motor fluctuations in Parkinson?s disease. [35] Ahmed I, Bose SK, Pavese N, et al. Glutamate NMDA receptor dysregulation in Parkinson?s disease with dyskinesias. [35] Tseng MT, Lin CH. Pain in early-stage Parkinson?s disease: implications from clinical features to pathophysiology mechanisms. [35] What are you doing to beat Parkinson?s? Get involved to help raise funds and awareness for the 1 million Americans living with Parkinson?s disease. [21] Every nine minutes someone is diagnosed with Parkinson?s disease. [16] The tulip is the international symbol of Parkinson?s disease. [16] The most common form of Parkinsonism is Parkinson?s disease, which is characterized by tremors--especially of fingers and hand--rigidity of muscles, slowness of movements and speech, and a masklike face. [16] Scott NW, Macleod AD, Counsell CE. Motor complications in an incident Parkinson?s disease cohort. [35] Stahl SM. Mechanism of action of pimavanserin in Parkinson?s disease psychosis: targeting serotonin 5HT2A and 5HT2C receptors. [35] Stefano GB, Mantione KJ, Kralickova M, et al. Parkinson?s disease, L-DOPA, and endogenous morphine: a revisit. [35] Young Blood MR, Ferro MM, Munhoz RP, et al. Classification and characteristics of pain associated with Parkinson?s disease. [35]

Muller T, Riederer P, Grunblatt E. Determination of monoamine oxidase A and B activity in long-term treated patients with Parkinson disease. [35] Olanow CW, Damier P, Goetz CG, et al. Multicenter, open-label, trial of sarizotan in Parkinson disease patients with levodopa-induced dyskinesias (the SPLENDID Study). [35] Baggio G, Cherubini P, Pischedda D, et al. Multiple neural representations of elementary logical connectives. [35] In MS, the myelin sheath disappears in multiple areas, leaving a scar, or sclerosis. [14] Lastly, safinamide is another promising agent in treatment of levodopa-induced dyskinesia, and the molecule is likely to affect multiple systems as it has both dopaminergic and non-dopaminergic effects ( Figure 3 ). [35]

In addition to their original pharmaceutical use in lowering cholesterol, statins display multiple neuroprotective effects. [11] When a repurposed therapeutic such as Simvastatin, has multiple pleiotropic effects, all or any of which may be clinically beneficial, there sometimes comes a point when one may just acknowledge we cannot identify a clear therapeutic target (because there are so many positively-orientated candidate modes of action), and go ahead and test it in the clinic. [11] Below is our current interpretation (updated to October 2017) of the multiple cholesterol-independent biochemical mechanisms of action of Simvastatin as originally cited by Roy and Pahan in 2011 that we believe specifically support the biochemical, physiological and pharmaceutical reasons underpinning this innovative clinical trial. [11] This built on their earlier observation that Simvastatin similarly worked in synergy with PPAR-? to protect cellular damage caused by systemic inflammation in a model of multiple organ failure. [11] Chronic neuroinflammation is a common mechanism that is shared by multiple neurodegenerative diseases including AD and MS and is a general cause of the initiation and progression of neurodegeneration. [5]

J. J. Bright, "Curcumin and autoimmune disease," Advances in Experimental Medicine and Biology, vol. 595, pp. 425-451, 2007. [5] H. Braak and K. Del Tredici, "Where, when, and in what form does sporadic Alzheimer's disease begin?" Current Opinion in Neurology, vol. 25, no. 6, pp. 708-714, 2012. [5] P. Mecocci, U. MacGarvey, and M. F. Beal, "Oxidative damage to mitochondrial DNA is increased in Alzheimer's disease," Annals of Neurology, vol. 36, no. 5, pp. 747-751, 1994. [5] A. Nunomura, G. Perry, G. Aliev et al., "Oxidative damage is the earliest event in Alzheimer disease," Journal of Neuropathology & Experimental Neurology, vol. 60, no. 8, pp. 759-767, 2001. [5]

Annweiler C, Rolland Y, Schott AM, Blain H, Vellas B, Herrmann FR, et al. Higher vitamin D dietary intake is associated with lower risk of Alzheimer?s disease: a 7-year follow-up. [7] Gezen-Ak D, Dursun E, BilgiB, Hana?asi H, Ertan T, Gvit H, et al. Vitamin D receptor gene haplotype is associated with late-onset Alzheimer?s disease. [7]

Lehmann DJ, Refsum H, Warden DR, Medway C, Wilcock GK, Smith AD. The vitamin D receptor gene is associated with Alzheimer?s disease. [7] Annweiler C, Llewellyn DJ, Beauchet O. Low serum vitamin D concentrations in Alzheimer?s disease: a systematic review and meta-analysis. [7] Littlejohns TJ, Henley WE, Lang IA, Annweiler C, Beauchet O, Chaves PHM, et al. Vitamin D and the risk of dementia and Alzheimer disease. [7]

Farrer LA, Cupples LA, Haines JL, Hyman B, Kukull WA, Mayeux R, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. [7] Reitz C, Brayne C, Mayeux R. Epidemiology of Alzheimer disease. [7]

Daw EW, Payami H, Nemens EJ, Nochlin D, Bird TD, Schellenberg GD, et al. The number of trait loci in late-onset Alzheimer disease. [7] Ding H, Dhima K, Lockhart KC, Locascio JJ, Hoesing AN, Duong K, et al. Unrecognized vitamin D3 deficiency is common in Parkinson disease. [7] Kurata T, Miyazaki K, Kozuki M, Morimoto N, Ohta Y, Ikeda Y, & Abe K (2012) Atorvastatin and pitavastatin reduce senile plaques and inflammatory responses in a mouse model of Alzheimer?s disease. [11] Schindowski K, Belarbi K, Bu L. Neurotrophic factors in Alzheimer?s disease: role of axonal transport. [7] Huang W, Li Z, Zhao L, & Zhao W (2017) Simvastatin ameliorate memory deficits and inflammation in clinical and mouse model of Alzheimer?s disease via modulating the expression of miR-106b. [11] Using a mouse model of Alzheimer?s disease (AD), Kurata et al. found that, after 15-20 months of treatment, both Atorvastatin and Pitavastatin were protective of senile plaque formation, and that this protection was preceded by a reduction of proinflammatory events including levels both of activated microglia and TNF-?. [11]

Robert Wood Johnson offers several innovative treatments for Parkinson's, including the Gamma Knife, as well as Deep Brain Stimulation. [4] The combined treatment of bone marrow-derived MSCs and resveratrol in EAE MS model was shown to suppress proinflammatory cytokines IFN- ? and TNF- ? and increase anti-inflammatory cytokines IL-4 and IL-10, thus alleviating EAE symptoms. [5] Combined treatment of Methylprednisolone and MSCs-IFN ? had enhanced therapeutic effects on EAE mice. [5]

They substantiated their findings by conducting further sensitivity analyses and concluded that their results "suggest a decreased relative risk of PD in statin users as identified by a combined meta-analysis of eight observational studies?. [11] Because of the low incidence of PD, the authors felt distinctions among RR, HR, and OR could be ignored, allowing combined case-control and cohort studies, and calculated the summary Relative Risks and 95% CIs. [11]

They offered "mounting and strong evidence? that immune transformation can affect the pathogenesis of neurodegenerative diseases, and that modulation of the inflammatory response, while restoring a homeostatic immune system via immunopharmacological strategies, may lead to new therapeutic opportunities for PD and other neurodegenerative disorders. [11] A. Campbell, "The potential role of aluminium in Alzheimer's disease," Nephrology Dialysis Transplantation, vol. 17, supplement 2, pp. 17-20, 2002. [5] M. Kawahara and M. Kato-Negishi, "Link between aluminum and the pathogenesis of Alzheimer's disease: the integration of the aluminum and amyloid cascade hypotheses," International Journal of Alzheimer's Disease, vol. 2011, Article ID 276393, 17 pages, 2011. [5]

In the context of autoimmune diseases, administration of vitamin D prevented the onset of experimental autoimmune encephalomyelitis (EAE), a rodent model of MS. [7] In this section, we summarize the neurosteroid properties of vitamin D beyond Ca homeostasis in relation to neuroinflammatory, neurodegenerative, and autoimmune diseases. [7] Fernandes de Abreu DA, Eyles D, Fon F. Vitamin D, a neuro-immunomodulator: implications for neurodegenerative and autoimmune diseases. [7]

Suzuki M, Yoshioka M, Hashimoto M, Murakami M, Noya M, Takahashi D, et al. Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease. [7] Gao X, Simon KC, Schwarzschild MA, & Ascherio A (2012) Prospective study of statin use and risk of Parkinson disease. [11] Wahner AD, Bronstein JM, Bordelon YM, & Ritz B (2008) Statin use and the risk of Parkinson disease. [11]

Prospective studies and meta-analyses have demonstrated that low serum or plasma vitamin D levels increased the risk of dementia, cognitive impairment, impaired motor functions, and memory decline which are all characteristics of neurodegenerative diseases. [7] The impact of vitamin D has been studied in cardiovascular diseases, neuroinflammation, and neurodegenerative diseases among others. [7] Vitamin D deficiency presumably plays a causative role in the pathogenesis and course of various neuroinflammatory and neurodegenerative diseases. [7]

Synthetic drugs and natural compounds such as polyphenols are being used for their potential stimulatory effect on stem cells against neurodegenerative diseases. [5] We add to this 2011 list, the topic of the stimulation of increased expression of neurotrophic factors by statins which was not covered by Roy & Pahan in 2011 but since then, in the context of neurodegenerative diseases, has shown also to be of considerable relevance to the other pleliotropic effects of statins mentioned above. [11]

MS is primarily a neurodegenerative disease as it involves the progressive degeneration of the grey and white matter resulting in atrophy of the brain and spinal cord. [5] Landfield PW, Thibault O, Mazzanti ML, Porter NM, Kerr DS. Mechanisms of neuronal death in brain aging and Alzheimer?s disease: role of endocrine-mediated calcium dyshomeostasis. [7] Corder EH, Saunders AM, Strittmatter WJ, Schmechel DE, Gaskell PC, Small GW, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer?s disease in late onset families. [7] Alzheimer?s disease is a neurodegenerative disorder affecting mostly elderly persons resulting in cognitive decline and dementia. [7] Most of the studies that have investigated the role of vitamin D in Alzheimer?s disease were observational or genetic studies. [7] Taghizadeh M, Talaei SA, Djazayeri A, Salami M. Vitamin D supplementation restores suppressed synaptic plasticity in Alzheimer?s disease. [7]

Zhang F, Jiang L. Neuroinflammation in Alzheimer?s disease. [7] Gan L, & Johnson JA (2014) Oxidative damage and the Nrf2-ARE pathway in neurodegenerative diseases. [11] Nrf2 is a cytoprotective master regulator of the transcriptional response to oxidative stress; it has a rapid turnover, and its role in neurodegenerative diseases has been well described by Gan and Johnson, and its diversity of actions and control with respect to mitochondrial function were recently well reviewed by Holmstrom et al., and also by Dinkova-Kostova et al. [11] It is well known that vascular risk factors increase risk of dementia, and it would not be unreasonable to suppose that the same might hold true for other neurodegenerative diseases. [11]

Currently, doctors don't' know for sure what causes MS. It's not clear by this autoimmune disease develops in some people and not others. [10] For a long time, NMOSD were considered rare variants of MS; however, the seminal detection of a highly specific serum biomarker, antibodies to the astrocyte water channel aquaporin-4, in up to 80% of patients with a NMOSD phenotype, as well as subsequent immunological, biomarker, and imaging studies made clear that NMOSD is an autoimmune disease entity distinct from MS. [7] The inherent ability to control this response, so that its effect is beneficial, is limited, and correlates with an individual's inherent ability to resist autoimmune disease induction. [8] What it is: A chronic autoimmune disease that causes inflammation, pain and swelling and can damage the skin, joints and, in severe cases, internal organs. [9]

Roy A, & Pahan K (2011) Prospects of statins in Parkinson disease. [11] Bykov K, Yoshida K, Weisskopf MG, & Gagne JJ (2017) Confounding of the association between statins and Parkinson disease: systematic review and meta-analysis. [11] Lue L-F, Schmitz CT, Snyder NL, Chen K, Walker DG, Davis KJ, et al. Converging mediators from immune and trophic pathways to identify Parkinson disease dementia. [7]

Lee Y-C, Lin C-H, Wu R-M, Lin M-S, Lin J-W, Chang C-H, & Lai M-S (2013) Discontinuation of statin therapy associates with Parkinson disease: a population-based study. [11]

Vemuri P, Schl M. Linking amyloid-? and tau deposition in Alzheimer disease. [7]

In PD dementia, a combination of Lewy bodies and neurites in cortical, limbic and brain stem areas, Alzheimer disease pathology (cortical and striatal amyloid and Braak tau) and vascular disease are believed to be its pathological basis. [35] Gomperts SN, Locascio JJ, Rentz D, et al. Amyloid is linked to cognitive decline in patients with Parkinson disease without dementia. [35] Holloway RG, Shoulson I, Fahn S, et al. Pramipexole vs levodopa as initial treatment for Parkinson disease: a 4-year randomized controlled trial. [35] Goodarzi Z, Mrklas KJ, Roberts DJ, Jette N, Pringsheim T, Holroyd-Leduc J. Detecting depression in Parkinson disease: a systematic review and meta-analysis. [15] Combined rasagiline and antidepressant use in Parkinson disease in the ADAGIO study: effects on nonmotor symptoms and tolerability. [35]

The combined direct and indirect cost of Parkinson?s, including treatment, social security payments and lost income, is estimated to be nearly $25 billion per year in the United States alone. [21]

In another type of surgery, specific areas in the brain that cause Parkinson's symptoms are destroyed. [12] As it progresses, Parkinson's can cause difficulty walking and balancing. [13]

Many people who get Parkinson's develop a hunched posture and a shuffling step. [13]

Gordon PH. Amyotrophic lateral sclerosis: an update for 2013 clinical features, pathophysiology, management and therapeutic trials. [15] Ehrt U, Larsen JP, Aarsland D. Pain and its relationship to depression in Parkinson disease. [35] Pyatigorskaya N, Mongin M, Valabregue R, et al. Medulla oblongata damage and cardiac autonomic dysfunction in Parkinson disease. [35] Conte A, Khan N, Defazio G, et al. Pathophysiology of somatosensory abnormalities in Parkinson disease. [35]

Durif F, Debilly B, Galitzky M, et al. Clozapine improves dyskinesias in Parkinson disease: a double-blind, placebo-controlled study. [35] Ballanger B, Strafella AP, van Eimeren T, et al. Serotonin 2A receptors and visual hallucinations in Parkinson disease. [35]

Potts LF, Park ES, Woo JM, et al. Dual kappa-agonist/mu-antagonist opioid receptor modulation reduces levodopa-induced dyskinesia and corrects dysregulated striatal changes in the nonhuman primate model of Parkinson disease. [35] Schapira AHV, Chaudhuri KR, Jenner P. Non-motor features of Parkinson disease. [35] Samudra N, Patel N, Womack KB, et al. Psychosis in Parkinson disease: a review of etiology, phenomenology, and management. [35]

Causes of tremor include neurological disorders, neurodegenerative diseases, drugs, mercury poisoning, overactive thyroid and liver failure. [12] What is dementia? Learn about dementia disorders such as Lewy Body Dementia, Alzheimer's disease (AD), Vascular (multi-infarct) dementia (MID), and more. [12] Forgetting the name of a loved one may be a result of Alzheimer's disease or the second leading cause of dementia: vascular dementia. [13]

Many of the known genes are similar to those that have been identified in people with other autoimmune diseases as type 1 diabetes, rheumatoid arthritis or lupus. [17] Tissue inflammation and antibodies in the blood that fight normal components of the body and tissue in people with MS are similar to those found in other autoimmune diseases. [17]

It is recognised that neurodegenerative diseases demonstrate significant heterogeneity in clinical characteristics, especially so in MND, and that the proportion of different subtypes in each disease group may have affected the results. [15]

Disease modification: Treatments or interventions that affect the underlying pathophysiology of the disease and have a beneficial outcome on the course of a disease, for example Parkinson's. [26] The prevalence of Parkinson's in the U.K. is about one in 500 people, with a total of about 127,000 people living with the disease. [36] Population studies on the incidence of Parkinson's are important to scientists' understanding of the history of the disease, its progression, and the risk factors associated with it. [36] Parkinson's News Today is strictly a news and information website about the disease. [36] It contains dopamine neurons, and it is black due to the high concentration of neuromelanin within these neurons. (Parkinson's disease is characterized by the death of dopaminergic neurons in the substantia nigra pars compacta.) [26]

Alpha-synuclein also accumulates in multiple system atrophy (MSA) and in Lewy Body Disease. [26] There are some treatments for MS symptoms but there is no cure and the root cause of the disease is unknown. [24] There are some treatments to manage the symptoms, but as the disease progresses treatments no longer work. [24] Placebo: A simulated or inert form of treatment without known proven benefit on a symptom or a disease. [26] It has been investigated as a potential treatment for diabetic nephropathy and kidney diseases and as a disease modifying therapy in PD. [26]

Parkinson?s News Today is strictly a news and information website about the disease. [36] Biomarker: An early indicator that a person may have a disease, such as Parkinson?s. [26]

Dementia is a disease that affects the brain where patients experience memory loss and difficulties with thinking. [24] At least two-thirds of individuals with PD will have a clinically significant neuropsychiatric disorder during the course of their disease, and most will have more than 1 disorder concurrently (Table). [28] Syndrome: A group of symptoms that tend to occur together and which reflect the presence of a specific disorders or diseases. [26] The stages of disease, risk factors, and symptoms are well understood. [24] A biomarker, if present, could indicate that the person has a disease before symptoms of that disease appear. [26]

Gene therapy: The insertion of genes into an individual's cells and tissues to treat hereditary diseases where deleterious mutant alleles can be replaced with functional ones. [26] Dementia: A decline in cognitive function due to damage or disease in the brain beyond what might be expected from normal aging. [26] Our goal is to reduce the number of people that develop and die from disease and to promote optimal health. [24] The prevalence of the disease ranges from 41 people per 100,000 in the fourth decade of life to more than 1,900 people per 100,000 among those who are 80 and older. [36] The incidence of the disease, or the rate of newly diagnosed cases, generally increases with age, although it can stabilize in people who are older than 80. [36]

PPMI: Parkinson?s Progression Markers Initiative: a study launched in 2010 by Michael J Fox Foundation to find biomarkers for PD; s a landmark observational clinical study to comprehensively evaluate people with Parkinson?s disease and those at greater risk of developing the disease, as well as healthy controls. [26] "Metabolomic profiling can offer unique insight into many different diseases, both mechanistically and therapeutically," says study co-senior author Gary Siuzdak, PhD, senior director of TSRI's Scripps Center for Metabolomics and professor of chemistry, molecular and computational biology. [30] Within every prodrome is both the cause of and the cure for disease. [24] The disease can cause movement problems and issues such as hallucinations in addition to thinking and memory problems. [23]

Neuroprotection: Mechanisms within the nervous system that would protect neurons from dying due to a degenerative disease or from other types of injury. [26]

According to UCB, a global biopharma company focused on severe diseases with operations in approximately 40 countries, there are over 100,000 Canadians living with Parkinson?s disease today, with about 6,600 new cases of Parkinson's diagnosed each year in Canada (based on an annual incidence of 20 new cases per 100,000 people). [36] With homozygous (both alleles affected) PINK-1 mutations, juvenile or early onset Parkinson?s disease can develop. Lack of PINK-1 causes an overload of calcium in mitochondria and indirectly cell death. [26] Synucleinopathy: A class of neurodegenerative disease resulting from pathological accumulation of alpha-synuclein in neurons (Parkinson?s, Lewy Body Dementia) or a kind of glia cells called oligodendrocytes (Multiple System Atrophy). [26] In Parkinson?s disease, it is believed that accumulation of damaged proteins "choke" the cell, leading to the eventual death of the cell. [26] Braak Staging: A method to classify the degree of pathology in Parkinson?s disease on brain autopsy, based on the idea that more brain regions contain alpha-synuclein pathology as Parkinson?s disease progresses over time. [26] An estimated seven to 10 million people worldwide have Parkinson?s disease. [36] Movement Disorder Speciailist (MDS): A neurologist that has special interest in and extra training and experience with movement disorders such as Parkinson?s disease. [26] DJ-1: Mutations in this gene cause an autosomal recessive form of Parkinson?s disease. [26] Several different mutations in the LRRK2 gene have been found to cause Parkinson?s disease, but there may also be variants within the general population that do not necessarily cause disease. [26] Used to treat mild to moderate dementia in Parkinson?s disease. [26] In Parkinson?s disease, there is a clumping of many proteins inside neurons, including alpha-synuclein. [26] Coenzyme Q10: An antioxidant studied in Parkinson?s disease to slow down disease progression, but with little proven benefit so far. [26] They can be used in both the early and late stages of Parkinson?s disease. [26] Nicotine is present in cigarette smoke and has been proposed to decrease chances of developing Parkinson?s disease, but this remains controversial and the mechanism of the relationship is not well understood. [26]

Deep brain stimulation of the GPi causes an increase in motor function in Parkinson's patients. [26] The substantia nigra, which is damaged in Parkinson's, is located in the midbrain of the brain stem. [26]

They found that a drug used to treat seizures may effectively treat the movement symptoms in people with dementia with Lewy bodies without causing additional psychiatric symptoms when combined with the Parkinson's drug levodopa. [23] A drug commonly used to treat movement symptoms in Parkinson's, levodopa, may worsen psychiatric symptoms in those with dementia with Lewy bodies, especially when higher doses are given as the effects of levodopa start to wane. [23] Dopamine antagonists can worsen Parkinson's symptoms and can cause drug-induced Parkinsonism. [26]

The FDA has approved Osmolex ER for adults with Parkinson's as well as drug induced extrapyramidal reactions. 3 Parkinson's is a neurodegenerative motor disorder characterized by tremor, rigidity, and problems with gait. [29] Gene therapy can also be used to correct non-genetic deficiencies such as the loss of dopamine in Parkinson's, to modify the function of a group of cells (e.g. convert an excitatory structure to one that is inhibitory) or to provide a source of growth factors. [26] Some growth factors are being looked at to try to promote the survival of the neural cells that are degenerating in Parkinson's. [26]

"Taurine lends hand to repair cells damaged in multiple sclerosis." [30] Multidisciplinary care: Care given by multiple healthcare professionals each approaching the patient from their professional perspective, often involves separate, individual consultations. [26]

The combined direct and indirect costs of Parkinson?s in the U.S. including treatment, disability, and similar costs, plus lost income from an inability to work, are estimated at $25 billion per year. [36] An estimated 4 percent of people with Parkinson's are diagnosed before age 50. [36] Communication between physician and caregivers is essential because the person with Parkinson's may not always be aware of symptomatic side effects of Osmolex ER. [29]

Weiss H, Marsh L. Impulse control disorders and compulsive behaviors associated with dopaminergic therapies in Parkinson disease. [28] Mosley PE, Moodie R, Dissanayaka N. Caregiver burden in Parkinson disease: a critical review of recent literature. [28]

MINNEAPOLIS - New help may be on the way for people with dementia with Lewy bodies, which is the second most common neurodegenerative type of dementia after Alzheimer's disease. [23] King LA, Horak FB. Delaying mobility disability in people with Parkinson disease using a sensorimotor agility exercise program. [27] Ffytche DH, Creese B, Politis M, et al. The psychosis spectrum in Parkinson disease. [28]

Tauopathies: A class of neurodegenerative diseases resulting from the pathological aggregation of tau protein in so-called neurofibrillary tangles (NFT) in the human brain. [26]

Parkinson's symptoms manifest differently in different patients; where patients experience some symptoms and not others, and even the pace at which the disease worsens varies on an individual basis. [32] The majority of Parkinson's patients are treated with medications to relieve the symptoms of the disease. [32]

A new breast cancer risk-prediction model combining histologic features of biopsied breast tissue from women with benign breast disease and individual patient demographic information more accurately classified breast cancer risk than the. [37] The risk of PD increases with age, so analysts expect the financial and public health impact of this disease to increase as the population gets older. [32]

While the condition usually develops after the age of 55, the disease may affect people in their 30s and 40s, such as actor Michael J. Fox, diagnosed at age 30. [32] These clinical trials are experiments that are testing, often for the first time ever in people, a whole new way of treating disease. [38]

It is much like the cardiologist who manages heart disease with medical intervention and the cardiac surgeon who offers surgery for those who have failed treatment with medications. [32] The discovery of the gene-editing tool CRISPR has opened up all sorts of possible new ways of developing treatments for deadly diseases. [38]

Slightly more men are diagnosed with PD than women - for every 3 men there are 2 women with the disease. [32] The progression of symptoms is often a bit different from one person to another due to the diversity of the disease. [25] A diagnosis of chronic obstructive pulmonary disease (COPD) in older adults was associated with increased risk of mild cognitive impairment (MCI), especially MCI of skills other than memory. [39] It is generally believed that the disease is a result of a combination of both genetic and environmental causes. [32]

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