It has been reported that loss of neuromuscular junctions (NMJs) is one of the earliest pathologies observed in ALS. In a recent article published in Cell Reports, researchers at the NYU School of Medicine reported that muscle skeletal receptor tyrosine kinase, MuSK, may help delay NMJ loss. When MuSK expression was increased 3-fold in an SOD1 G93A mouse, it delayed the onset of muscle denervation by nearly 40 days. Although MuSK overexpression was not linked to an increase in lifespan, it does provide a potential opportunity to improve the quality of life for people with ALS by allowing them to maintain control of their muscles for longer. Read more about the MuSK story here.
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