Blocking the protein receptor, muscarinic type 3, may be effective in promoting remyelination in patients with multiple sclerosis.
This article originally appeared on The American Journal of Managed Care.
Multiple sclerosis (MS) involves the progressive loss of the protective layer of nerve fibers, myelin, and its loss, called demyelination, results in symptoms of MS. Blocking the protein receptor, muscarinic type 3 (M
R), may be effective in promoting remyelination in patients with MS, based on the results of a study
published by the Journal of Neuroscience.
Triggering remyelination results in the formation of new myelin sheaths and plays a significant role when developing effective MS treatments. The process of remyelination is spontaneous, but involves the transformation of oligodendrocyte progenitor cells (OPCs) into oligodendrocytes.
Previous research has demonstrated that muscarinic receptors (MR) can bind the neurotransmitter acetylcholine, and can induce the differentiation of OPCs, and, therefore, speed remyelination.
“The identification of drug targets aimed at improving remyelination in patients with demyelination disease is a key step in development of effective regenerative therapies to treat diseases such as multiple sclerosis,” the authors wrote. “Muscarinic receptor antagonists have been identified as effective potentiators of remyelination but the receptor subtypes that mediate these receptors are unclear.”
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