Multiple Sclerosis (MS) is a degenerativedisease that primarily affects the Central Nervous System (CNS)1.There are a variety of theories pertaining to the cause of MS and there iscurrently no cure available.
Although there is no cure, treatments may helpreduce the effects of symptoms and slow progression of the disease. With thisautoimmune disease, multiple lesions are usually found on the brain/spinal cordwhich in turn affect neural transmission. These lesions can slow down or blockneural transmission, leading to weakness, sensory loss, and other neurologicalsymptoms. Currently, there are 4 recognizable subtypes of MS, these includeRelapsing Remitting MS (RRMS), Secondary Progressive MS (SPMS), PrimaryProgressive MS (PPMS) and Progressive Relapsing MS (PRMS). RRMS ischaracterized by relapsing periods of neurological dysfunction that can lastfrom days to months followed by a partial/full recovery.
The recovery period isoften a very stable time in between the relapses. Similarly, SPMS initiallybegins as a relapse/remission pattern that eventually changes into a steadyprogression of the disease. On the other hand, PPMS is a continuous decline ofneurologic function with minimal recovery. Lastly PRMS consists of periods ofrelapses with minimal recovery, resulting in the disease progressively gettingworse from the onset.Multiple Sclerosis is a commoninflammatory disease and can result in demyelination, axon loss andinflammation2.The CNS is responsible for integrating and responding to the sensoryinformation received from the body and it consists of the brain & spinalcord.
Nerves cells are the specialized cells involved in the CNS anddemyelination involves the breakdown of the myelin sheath thatsurrounds/insulates these nerve cells. It can be due to the direct damage tomyelin by inflammatory cells which results in neurons being more susceptible toapoptosis. By losing its myelin sheath, neurons become more susceptible to thebinding of agents that induce apoptosis.In contrast to demyelination, themechanisms that underlie the progression of axon loss are currently unknown.3Theories for causes of axonal damage include direct cytotoxic attack, antibodymediated lesion, or exposure to glutamate. Moreover, it has been discoveredthat acute damage to the axon occurs mostly in the early stages with a tendencyto slow as the disease progresses and has been linked to chronic disabilitiesin those with MS4. Similarly, the inflammatory aspect of MS has alsobeen linked to functional disability and is primarily the result of theoverproduction inflammatory cytokines.
Autoreactive T-Cells stimulatemicroglial, astrocytes and antibody production while also secreting thecytokines that recruit inflammatory cells4.Microglial cells are similar to macrophages in which they destroy cellsperceived to be pathogenic and remove damaged cells. Alternatively, the role ofastrocytes in MS is a poorly understood mechanism, however there are severalsuggested mechanisms that could contribute to MS. These mechanisms includeastrocytes being a part of the innate immune system, a source of cytotoxicfactors, an inhibitor to remyelination or a contributor to axonal mitochondrialdysfunction5.Anti-myelin antibodies in addition to microglial cells and astrocytes, each contributeto produce demyelination of the nerve cells.
To sum up,Multiple Sclerosis is a degenerative disease that affects the nerve cells ofthe Central Nervous System. Despite not having a cure, treatments for MS havebeen able to combat symptoms and slow progression of the disease. MS can bediagnosed via MRIs and can affect regions of the brain & spinal cord,resulting in demyelination, axon loss and inflammation. With proper medicaltreatment and physical therapy, symptoms such as fatigue, pain, balance anddepression can be controlled and managed.