Neurologic autoimmune diseases

Neurological autoimmune diseases (NADs) are characterized by an aberrant immune response against antigens in the central nervous system or peripheral nervous system (PNS). The wide spectrum of these diseases depends on an individual’s ancestry, immunopathology, and mechanism of injury. Some of the most important autoimmune neurological syndromes include multiple sclerosis, neuromyelitis optica (NMO), Guillain–Barré syndrome, chronic inflammatory demyelinating polyneuropathy, myasthenia gravis (MG), autoimmune encephalitis, and paraneoplastic neurological disorders (PNDs). Patients experience different neurological manifestations based on the localization of the disease process. The importance of NADs is related to an increase in physician awareness of these diseases. Given the large number of diseases described and the plentiful number of factors that are associated with an autoimmune response, the identification of a common immunopathological mechanism that can explain NADs is a challenge. Among the factors studied, previous infections, genetic predisposition, cancer, vitamin D metabolism, and microbiota have been identified. Autoantibodies to various self-antigens have been shown to occur in many of these diseases, including antimyelin oligodendrocyte glycoprotein and antiaquaporin 4 in NMO, anti-N-methyl-d-aspartate receptor in AIE, antiacetylcholine receptor in MG, and others. A genetic component to the pathogenesis is supported by the identification of human leukocyte antigen associations in patients with NADs. Other possible pathogenic mechanisms include molecular mimicry, CD4+ activation, and CD8+ cytotoxicity. Treatment of NADs on reversing the inflammatory pathway activation present in many of these diseases; however, not all forms of immunosuppressive are equally effective. Future research focusing on identifying the roles of genetics and epigenetics in the pathogenesis will help to develop targeted therapies and a more personalized approach to management.