WHAT? Multiple sclerosis (MS) is a complex multifactorial disease that results from the interplay between environmental factors and a susceptible genetic background. This disease attacks patients at the neurological level and through a series of critical events (relapses) that take place at unpredictable time intervals, the patient’s health deteriorates (disability progresses). The idea is to delay relapses so we can manage the disease better for improved quality of life and for a longer period of time.
Together, these factors trigger a cascade of events involving the engagement of the immune system, inflammatory injury of myelin, axons and glia, functional recovery and structural repair, gliosis and neurodegeneration. The mechanisms involved include immune mediated inflammation, oxidative stress and excitotoxicity, all of which contribute to oligodendrocyte and neuronal damage and even cell death, hence promoting disease progression. The increasing prevalence of MS, combined with the partial efficacy and side effects of the existing treatments, have urged the development of new, innovative, more effective, safe and preventive treatment strategies.
For most people with MS, the disease slowly progresses with a series of unpredictable relapses (attacks of neurological symptoms). But for some, the progression of the disease is rapid. Relapses often lead to increasing and severe disabilities such as walking impairment, muscle weakness, speech or vision impairments and many others. More than 50% of the relapsing MS patients will eventually develop severe handicaps 10-15 years after the onset of the disease.
85% of the patients initially diagnosed are experiencing clearly defined relapses followed by periods of partial or complete recovery or remission; the Relapsing/Remitting (RRMS) type of the disease. Most RRMS patients enter a secondary progressive phase and accumulate irreversible neurological deficits that lead to some type of disability. The primary progressive is the type of the disease where patients are experiencing progression of disability without relapses.
WHY? The disease is characterized as Complex Multifactorial since multiple environmental and biochemical factors/processes are simultaneously orchestrated for the pathogenesis of the disease (an interconnected dynamic network of events). These factors trigger a cascade of events such as autoimmunity, acute inflammatory injury of myelin, axons and glia, neurodegeneration and structural repair. All these lead to the distraction of the central nervous system.
The polyunsaturated fatty acid (PUFA) composition of membrane phospholipids plays an important role in immune-related and non-immune-related inflammation. PUFA and antioxidant deficiencies, along with decreased cellular antioxidant defense mechanisms, have been reported in MS patients. The cause of PUFA deficiencies is not entirely clear and may involve metabolic and nutritional alterations. Increased or uncontrolled inflammation contributes to several different acute and chronic diseases, and it is characterized by the production of inflammatory cytokines, arachidonic acid (AA)-derived eicosanoids (prostaglandins (PGs), thromboxanes (TXs), leukotrienes ((LTs) and other oxidized derivatives) and other inflammatory agents such as reactive oxygen species (ROS), nitric oxide (NO) and adhesion molecules. During inflammation, glutamate homeostasis is altered by the release of increased quantities of glutamate by activated immune cells, which can result in the over activation of glutamate receptors and, in turn, excitotoxic oligodendroglial death. Among others, membrane-related pathology, immune-mediated inflammation, oxidative stress and excitotoxicity provide potentially useful combined targets for intervention in MS.
WHO? MS is an Autoimmune, multifactorial chronic, unpredictable and progressive disease of the central nervous system that attacks relatively young patients between the ages of 20 and 40 years old. It Induces inflammation and destruction of the myelin sheath, the protective layer that surrounds the body’s nerve fibers. Myelin is predominately lipid (~80%) consisting mostly of PUFA-lipids (DHA) as the major component.
