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. 2020 Dec 10;12:597811. doi: 10.3389/fnagi.2020.597811

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Copyright © 2020 Bao, Cui, Chow, Qin, Wong and Cheung.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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AChRs morphological degeneration and functional adaptations during aging. Increased endplate fragmentation and denervation during aging disrupt precise neurotransmission at NMJ. To compensate and recover normal function, slow-twitch muscles and fast-twitch muscles mainly composed of MHC IIb tend to increase ACh quanta releasing, while skeletal muscles mainly composed of MHC IIa would increase AChE activity and the affinity between AChRs and ACh. Ach, acetylcholine; AChR, acetylcholine receptor; AChE, acetylcholinesterase.