Jasutkar Hilary Grosso, Yamamoto Ai
Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854.
Departments of Neurology and Pathology and Cell Biology, Columbia University, New York, NY 10032.
Curr Opin Physiol. 2023 Apr;32. doi: 10.1016/j.cophys.2023.100631. Epub 2023 Jan 20.
Macroautophagy, herein referred to as autophagy, has long been implicated in the pathophysiology of neurodegenerative diseases. However, an incomplete understanding of how autophagy contributes to disease pathogenesis has limited progress in acting on this potential target for the development of disease modifying therapeutics. Research in the past few decades has revealed that autophagy plays a specialized role in the synapse, a site of early dysfunction in multiple neurodegenerative diseases. In this review we discuss the evidence suggesting that inadequate autophagy at the synapse may contribute to neurodegeneration, and why the functions of autophagy may be particularly relevant for synaptic function.
巨自噬,在本文中简称为自噬,长期以来一直被认为与神经退行性疾病的病理生理学有关。然而,对于自噬如何促成疾病发病机制的理解不完整,限制了针对这一潜在靶点开发疾病修饰疗法的进展。过去几十年的研究表明,自噬在突触中发挥着特殊作用,而突触是多种神经退行性疾病早期功能障碍的部位。在这篇综述中,我们讨论了相关证据,这些证据表明突触处自噬不足可能导致神经退行性变,以及为什么自噬的功能可能与突触功能特别相关。