The Fulcrum of Demyelination in Multiple Sclerosis

Author:

Ganesan Abinaya12,Muralidharan Pooja12,Ramya Lakshmi Narasimhan2

Affiliation:

1. Department of Biotechnology, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India

2. Computational and Molecular Biophysics Laboratory, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India

Abstract

Abstract: Multiple sclerosis (MS) is an autoimmune disorder that affects the central nervous system (CNS), including the brain, spinal cord, and optic nerves. The symptoms can vary from muscle weakness to vision loss. In the case of MS, the immune system attacks the myelin sheath, which protects the nerve fiber and causes inflammation resulting in demyelination. The myelin sheath has the composition of various proteins including membrane proteins and glycoproteins. The four main proteins namely Myelin Basic Protein (MBP), Myelin associated Oligodendrocyte Basic protein (MOBP), Myelin Proteolipid Protein (PLP) and Myelin Associated Glycoprotein (MAG) are known to be critical auto-antigens in causing demyelination in CNS leading to MS. Three out of these four proteins are intrinsically disordered proteins and in this review, we attempted to understand how these proteins play a crucial role in maintaining the integrity of myelin, by exploring its structural and functional aspects and also their auto-antigenicity leading to multiple sclerosis.

Publisher

Bentham Science Publishers Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry,General Medicine

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