The unfolding landscape of the congenital myasthenic syndromes

Ann N Y Acad Sci. 2018 Feb;1413(1):25-34. doi: 10.1111/nyas.13539. Epub 2018 Jan 21.

Abstract

Congenital myasthenic syndromes (CMS) are heterogeneous disorders in which the safety margin of neuromuscular transmission is impaired by one or more specific mechanisms. Since the advent of next-generation sequencing methods, the discovery of novel CMS targets and phenotypes has proceeded at an accelerated rate. Here, we review the current classification of CMS and describe our findings in five of these targets identified and investigated in our laboratory in the past 5 years. Defects in LRP4 hinder synaptic development and maintenance; the defects in PREPL are predicted to diminish filling of the synaptic vesicle with acetylcholine; and defects in SNAP25, Munc13-1, and synaptotbrevin-1 impede synaptic vesicle exocytosis.

Keywords: LRP4; Munc13-1; PREPL; SNAP25B; congenital myasthenic syndromes; synaptobrevin.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Acetylcholine / metabolism
  • Humans
  • LDL-Receptor Related Proteins / genetics
  • Myasthenic Syndromes, Congenital / genetics*
  • Myasthenic Syndromes, Congenital / pathology*
  • Nerve Tissue Proteins / genetics
  • Neuromuscular Junction / pathology*
  • Prolyl Oligopeptidases
  • R-SNARE Proteins / genetics
  • Serine Endopeptidases / genetics
  • Synaptic Transmission / physiology*
  • Synaptosomal-Associated Protein 25 / genetics

Substances

  • LDL-Receptor Related Proteins
  • LRP4 protein, human
  • Nerve Tissue Proteins
  • R-SNARE Proteins
  • SNAP25 protein, human
  • Synaptosomal-Associated Protein 25
  • UNC13B protein, human
  • Serine Endopeptidases
  • PREPL protein, human
  • Prolyl Oligopeptidases
  • Acetylcholine