Multiple Sclerosis

Multiple sclerosis (MS), a chronic autoimmune disease, is a potent case of how detrimental an imbalance in the relationship between the central nervous system and our functioning can be. A mistake in the immune system’s functioning in individuals who develop MS leads to an attack on the central nervous system. The protective fatty material, called myelin, which sheaths the nerve fibers of the all too important brain and spinal cord, are subject to an unrelenting attack by the body’s very own defense mechanisms. As a consequence, inflammation persists and limits the effectiveness of the communication between one’s body and brain. This is because the normal flow of electrochemical impulses, that travel along the central nervous system’s nerve fibers are disrupted by the inflammatory conditions. Gradually, the nervous system is unable to recover, and effectively salvage its functioning as scarring sets in. The progression of these changes vary among the cases of MS. Four distinct classifications have been recognized; progressive relapsing MS which makes up about five percent of cases, primary progressive MS which makes up about ten percent of cases, relapsing-remitting MS which makes up about eighty-five percent of cases, and secondary progressive MS which develops later on in the majority of individuals initially affected with relapsing-remitting MS. Despite these differences in the progression of MS, the disease culminates into a state of progressive disability that ultimately limits an individual’s ability to function in their everyday lives. The study of MS presents an undeniable opportunity for the field of neuroscience to enrich its understanding of how the many components of our internal and external environments link together. In gaining further knowledge about the mechanisms responsible for the propagation of MS, neuroscientists look to epidemiology and genetics[1] and nutrition as external factors; neuropathology as a way to gain valuable insight into the pathogenesis of MS; treatments, specifically for the most prevalent form, relapsing-remitting MS, as a way to combat the disease’s progression; and controversial theories, such as Chronic Cerebrospinal Venous Insufficiency, that attempt to explain the underlying mechanisms[2].

1. Wakerley, B., Nicholas, R. & Malik O. Multiple sclerosis. Medicine 40, 523-528 (2012).
2. Morovic, S. & Zamboni, P. CCSVI is associated with multiple sclerosis. Neurol Res. 34, 770-779 (2012).

1. Epidemiology & Genetics of Multiple Sclerosis

main article: 1. Epidemiology & Genetics of Multiple Sclerosis
author: Stephan Jayaratnam
Multiple Sclerosis (MS) is a chronic autoimmune disease affecting the myelinated axons of the central nervous system; for those with MS, myelin sheaths are destroyed by one’s immune system, leading to a deficiency in the communication between one’s body and brain. There are four different types of MS including primary progressive MS, progressive relapsing MS, relapsing-remitting MS and secondary progressive MS. The epidemiology of MS covers sex ratios and the age statistics of MS, as well as prevalence rates, incidence rates and geographical differences. For example, prevalence of MS increases the farther you move away from the equator, suggesting links to sunlight exposure[1]. Tying into epidemiology is the investigation of the role of genetics in MS development. Those with two or more close relatives (parents or siblings) with MS are 40 times more likely to develop MS than someone without affected relatives[1]. Also, a few genetic factors have been linked to MS, most notably the role of the Human Leukocyte Antigen (HLA). Certain HLA types have been hypothesized to play a role in the malfunctioning of the immune system which leads to the destruction of myelin proteins by one’s own T-Cells[1].

1. Wakerley, B., Nicholas, R., Malik O. Multiple sclerosis. Medicine 40, 523-528 (2012).

2. Management of MS symptoms with Nutrition

main article: 2. Management of MS symptoms with Nutrition
author: Gabrielle Messier

Polyphenol-rich Berries
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Polyphenols have shown benefits in EAE mouse models[3][Bibliography item Picture1 not found.].

Multiple Sclerosis has no cure. Inflammation-dependent relapse is treated with Conventional Therapies such as interferon beta injection, but these do not treat every MS symptom and often come with unpleasant side effects. Diets and supplementation are employed by 50 to 75% of individuals with MS as symptom management tools[1][2].The following are a selection of the vitamins, minerals, fatty acids, and dietary practices under investigation to relieve MS symptoms.

1. Gaby, A. Multiple Sclerosis. Glob Adv Health Med. 2(1), 50-56 (2013).
2. Farinotti et al. Dietary Interventions for multiple Sclerosis (Review). The Chohrane Library. 12. 1-50 (2012).
3. Geldern, G. and Mowry E. The influence of nutritional factors on the prognosis of multiple sclerosis. Nat. Rev. Neurol. 8, 678-689 (2012).

3. Neuropathology of Multiple Sclerosis

main article: 3. Neuropathology of Multiple Sclerosis
author: Megan Steeves

Figure 1. Atrophy of the Brain in MS
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An individual with MS was followed for a period of 18 months.
During this time, significant atrophy in the brain was observed.

"I've had MS since 1975. I don't know how many relapses I've had. I don't know what all my symptoms are. That is the problem. MS wears many masks." - Anonymous MS Patient Source:

Multiple sclerosis (MS) is a debilitating disease that imposes vast limitations on an individual’s ability to function in their everyday life, primarily as a consequence of the associated effects of demyelination of the central nervous system. To explain the pathogenesis of MS, neuroscientists have traditionally focused their efforts on understanding white matter pathology. White matter pathology has been found to be characterized by such features as focal demyelinated plaques that are often associated with a host of inflammatory pathways [1]. However, recent advancements in the field of neuropathology have allowed for the closer examination of grey matter tissues and its correlation with the disease symptoms of MS. Closer examination of the grey matter pathology of MS has revealed characteristic features that allow them to be distinguishable from that of white matter [1]. These differences suggest that the disease phenotype presented in MS must be a result of the combinatorial effects of both types of neural tissue changes. Moving forward, it is only by gaining a deeper understanding of the changes in both the white and grey matter of the brain that we are able to sufficiently explain the deficits shown in individuals with MS.

1. Geurts, J., Barkhof, F. Grey matter pathology in multiple sclerosis. Lancet Neurology. 7, 841-851 (2008).

4. Relapsing Remitting Multiple Sclerosis Treatments

main article: 4. Relapsing Remitting Multiple Sclerosis Treatments
author: Matthew Meehan
Multiple Sclerosis (MS) is a central nervous system (CNS) autoimmune disease where axons are targeted by the immune system leading to degradation of the myelin sheaths around them. By destroying these sheaths, the axons of the CNS become far less capable in their ability to transmit signals, causing faulty or absent communication between neurons. In the majority of MS cases, an initial phase of the disease is experienced, followed later by a series of relapses and remissions, this form of MS is aptly named Relapsing-Remitting MS (RRMS)[1]. In the relapse events of RRMS, demyelination occurs in an inflammatory autoimmune attack in the CNS which may cause lasting damage, and having many of these events over years can lead to a variety of disabilities[1]. It is clear that treating these relapse events as effectively as possible is critical to improving a patient’s long-term health and functionality. As a first line of treatment for RRMS relapses several medications are available, though the main ones used are interferon-βs and glatiramer acetate[1]. Both of these medications serve a similar function in the attempt to remedy the autoimmune attack, and that is by decreasing inflammation in a variety of ways, mainly through interactions with the body’s T-cells[1]. The precise mechanisms of the pathways involved in these treatments are not fully known though, and research on their effectiveness and treatment regimens continues to be done.

1. Castelli-Haley J., Oleen-Burkey M.K.A., Lage M.J., and Johnson K.P. Glatiramer acetate versus interferon beta-1a for subcutaneous administration: comparison of outcomes among multiple sclerosis patients. Advances in Therapy 25, 658-673 (2008).

5. Chronic Cerebrospinal Venous Insufficiency

main article: 5. Chronic Cerebrospinal Venous Insufficiency
author: Dasiga Sundaralingam
Chronic Cerebrospinal Venous Insufficiency, more commonly known as CCSVI, is a vascular disease that results from the narrowing of the internal jugular and azygos veins (stenosis). This leads to a disruption to the blood flow from the brain and spinal cord. In 2006, Dr. Zamboni argued that there was an association between CCSVI and Multiple Sclerosis (MS) [1]. He stated that because the blood could not be drained from the brain and spinal cord, this deposits iron in the central nervous system, triggering autoimmunity [1]. He stated that endovascular surgery, also known as liberation therapy, showed dramatic improvements in symptoms within his MS patients. In this therapy, blood was drained from the brain and spinal cord by opening up the internal jugular and azygos veins. However, there has been major controversy to this original paper where many scholars have argued that his study was not blinded and had no control groups. They emphasized that due to these research methodological insufficiencies, a conclusive argument could not be made about the association between CCSVI and MS, and therefore liberation therapy should be approached with caution [2].

1. Zamboni, P. (2006). The big idea: iron-dependent inflammation in venous disease and proposed parallels in multiple sclerosis. Journal of the Royal Society of Medicine, 99: 589-593.
2. Morovic, S., & Zamboni, P. (2012). CCSVI is associated with multiple sclerosis. Neurological Research, 34(8): 770-779.

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