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- W2891839124 abstract "A properly functioning neuromuscular junction (NMJ) is essential for locomotion and overall health. The molecular mechanisms of NMJ formation are well established. This process is coordinated by the extracellular matrix molecule agrin, which activates a downstream signaling pathway via the Lrp4-MuSK-Dok7 complex, which in turn triggers the organization of rapsyn-AChR complexes. Highlighting their importance in NMJ maintenance, mutations in genes coding for these molecules cause congenital myasthenic syndrome. Correlative evidence indicates that NMJ structure also deteriorates in sarcopenia, the age-related loss of muscle mass and function. Sarcopenia is the primary cause of frailty and a major contributor to morbidity in the elderly. However, it is unclear whether age-related structural changes to the NMJ reflect changes in NMJ function. Moreover, the molecular mechanisms responsible are yet to be elucidated. We will summarize the current evidence for a functional role of NMJ maintenance in sarcopenia and present data indicating the involvement of the mammalian target of rapamycin (mTOR) pathway. Specifically, we find that sustained activation of mTORC1 de-stabilizes mouse NMJs and impairs neuromuscular transmission. In addition, muscle denervation rapidly precipitates the myopathy in young mice with sustained mTORC1 activation in skeletal muscle. These results suggest that tight control of mTORC1 signaling within myofibers is important for the maintenance of proper NMJ function throughout life." @default.
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- W2891839124 date "2018-10-01" @default.
- W2891839124 modified "2023-09-27" @default.
- W2891839124 title "NEUROMUSCULAR JUNCTION DEFECTS" @default.
- W2891839124 doi "https://doi.org/10.1016/j.nmd.2018.06.021" @default.
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