[Myasthenia gravis and acetylcholine].

A century has passed since the discovery of the first neurotransmitter, acetylcholine, in 1914. Extensive research on acetylcholine and its function has provided us with important options to treat the formerly intractable neuromuscular disease myasthenia gravis (MG). In the first days of treatment for MG, acetylcholine esterase inhibitors are administered, which is only a symptomatic therapy. After overwhelming developments in immunology, the immunological mechanisms of MG at the molecular or genetic level were recognized. Destruction of the acetylcholine receptors through autoimmune attacks plays a pivotal role in the evolution of MG. Thus, a mainstay of the newly developing treatments for MG are effective immunosuppression or immunomodulation. However, these therapeutic approaches are still "symptomatic", and target immunological rather than specific myasthenic symptoms. Immunomodulation may result in fatal immunodeficiency. From this point of view, although they are somewhat removed from first-line MG treatment (cholinesterase inhibitors), future drug development should focus on the cancellation of autoimmunity in MG patients.