SOD1 and amyotrophic lateral sclerosis: Later, McIntosh et al. showed in the SOD1-G93A mouse model of amyotrophic lateral sclerosis (ALS), as the delay in the MLR in DOMS was first proposed through an ALS-based theory [11], that abnormalities first evolve in neuromuscular junctions in the form of dysfunction, but later even postsynaptic structures detach from the neuromuscular junctions, and all happens before the appearance of ALS motor symptoms [27].