Novartis Institutes for Biomedical Research, Basel, Switzerland.
Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK.
Ann N Y Acad Sci. 2018 Jan;1412(1):41-53. doi: 10.1111/nyas.13521. Epub 2017 Dec 31.
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.
随着哺乳动物年龄的增长,它们的神经肌肉接点 (NMJ) 会改变其形态,轴突分支的系统变得越来越复杂,支配着越来越碎片化的突触后分化区域。有人认为这种重塑与神经肌肉传递的损伤有关,并且这导致了哺乳动物(包括人类)的与年龄相关的肌肉无力。在这里,我们回顾了以前关于 NMJ 老化的研究,其中大部分集中在结构或功能上,以及一项旨在寻找单个 NMJ 结构和功能之间相关性的新研究。虽然很明显,广泛的结构变化是衰老过程的一部分,但这些变化与功能障碍的相关性如何,甚至是否存在相关性,都还不太确定。这就留下了一个问题,即 NMJ 功能的丧失是否是与年龄相关的肌肉无力的一个重要原因。