Multiple Sclerosis (MS) is a chronic, immune-mediated demyelinating disease of the central nervous system (CNS) characterized by inflammation, neurodegeneration, and gliosis. It most commonly affects young adults, with onset typically between ages 20 and 40, and is approximately three times more prevalent in women than men. The hallmark pathology of MS includes focal inflammatory lesions with demyelination and axonal loss in the brain, spinal cord, and optic nerves, as well as diffuse neurodegeneration and atrophy in later stages.
MS is widely considered an autoimmune disorder, in which peripheral immune cells—particularly autoreactive T cells and B cells—gain access to the CNS through a compromised blood-brain barrier and initiate attacks against myelin sheaths and oligodendrocytes. Inflammatory cascades are further amplified by microglial activation and complement-mediated damage, while impaired remyelination and glial scar formation contribute to chronic disability. MS manifests in several clinical forms, most commonly relapsing-remitting MS (RRMS), which can evolve into secondary progressive MS (SPMS), and less frequently as primary progressive MS (PPMS). Although its precise cause remains unknown, MS susceptibility is influenced by genetic factors, such as HLA-DRB1 alleles, and environmental exposures, including Epstein-Barr virus infection, low vitamin D levels, and smoking.
Advances in imaging and immunopathology have greatly enhanced the understanding of lesion dynamics and CNS compartmentalization of immune responses. Disease-modifying therapies (DMTs) that modulate or suppress immune activity—such as interferons, monoclonal antibodies, and S1P receptor modulators—have transformed MS treatment, particularly in RRMS, but no curative therapies exist and neuroprotective strategies remain a critical area of investigation.
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