Development of abnormalities at the neuromuscular junction in the SOD1-G93A mouse model of ALS: dysfunction then disruption of postsynaptic structure precede overt motor symptoms

Development of abnormalities at the neuromuscular junction in the SOD1-G93A mouse model of ALS: dysfunction then disruption of postsynaptic structure precede overt motor symptoms

IntroductionThe ultimate deficit in amyotrophic lateral sclerosis (ALS) is neuromuscular junction (NMJ) loss, producing permanent paralysis, ultimately in respiratory muscles. However, understanding the functional and structural deficits at NMJs prior to this loss is crucial for therapeutic strategy...

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Bibliographic Details
Main Authors: Jayne McIntosh, Imane Mekrouda, Maryam Dashti, Claudiu V. Giuraniuc, Robert W. Banks, Gareth B. Miles, Guy S. Bewick
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-05-01
Series:Frontiers in Molecular Neuroscience
Subjects:
neuromuscular junction
motor neuron disease
neuromuscular transmission
SOD1-G93A
ALS
acetylcholine receptor
Online Access:https://www.frontiersin.org/articles/10.3389/fnmol.2023.1169075/full

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https://www.frontiersin.org/articles/10.3389/fnmol.2023.1169075/full

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