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
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DOI: 10.3389/fnmol.2023.1169075
Abstract: Introduction The 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… read more here.
Keywords: neuromuscular junction; sod1 g93a; motor symptoms; g93a mouse ... See more keywords