Paper Contents
Abstract
Myasthenia gravis (MG) is an auto immune neurological disorder characterized by defective transmission at the neuromuscular junction. The incidence of the disease is 4.1 to 30 cases per million person-years, and the prevalence rate ranges from 150 to 200 cases per million. MG is considered a classic example of antibody-mediated auto immune disease. Most patients with MG have autoantibodies against the acetylcholine receptors (AChRs). Less commonly identified autoantibodies include those targeted to muscle-specific kinase (MuSK), low-density lipoprotein receptor-related protein 4 (Lrp4), and agrin. These autoantibodies disrupt cholinergic transmission between nerve terminals and muscle fibers by causing downregulation, destruction, functional blocking of AChRs, or disrupting the clustering of AChRs in the postsynaptic membrane. The core clinical manifestation of MGisfatigable muscle weakness, which may affect ocular, bulbar, respiratory and limb muscles. Clinical manifestations vary according to the type of autoantibody, and whether a thymoma is present. The autoantibodies targeted neuromuscular junction (NMJ) molecules, such as nicotinic acetylcholine receptor (AChR), muscle-specific kinase (MuSK), and low-density protein related lipoprotein receptor 4 (Lrp4) that altera in tissue architecture and decrease the density or functionality of AChR and decrease neuromuscular transmission by various mechanisms. Therefore, a serious weakness of the fatigued skeletal muscle.
Copyright
Copyright © 2024 A. BINDU MADHAVI. This is an open access article distributed under the Creative Commons Attribution License.
