Abstract
As mammals age, their neuromuscular junctions (NMJs) change their form, with an increasingly complex system of axonal branches innervating increasingly fragmented regions of postsynaptic differentiation. It has been suggested that this remodeling is associated with impairment of neuromuscular transmission and that this contributes to age-related muscle weakness in mammals, including humans. Here, we review previous work on NMJ aging, most of which has focused on either structure or function, as well as a new study aimed at seeking correlation between the structure and function of individual NMJs. While it is clear that extensive structural changes occur as part of the aging process, it is much less certain how, if at all, these are correlated with an impairment of function. This leaves open the question of whether loss of NMJ function is a significant cause of age-related muscle weakness.
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