Graduate School of Life and Earth Sciences, University of Amsterdam, Science Park 904, 1090 GE Amsterdam, The Netherlands.
Department of Neurology, Columbia University Medical Center, New York, NY, USA; Center for Motor Neuron Biology and Diseases, Columbia University Medical Center, New York, NY, USA; Center for Genomics of Neurodegenerative Disease, New York Genome Center, New York, NY, USA.
Trends Neurosci. 2021 Aug;44(8):658-668. doi: 10.1016/j.tins.2021.04.008. Epub 2021 May 15.
Amyotrophic lateral sclerosis (ALS) is the most common adult-onset paralytic disorder, characterized mainly by a loss of motor neurons (MNs) in the CNS. Over the past decades, thanks to intense investigations performed in both in vivo and in vitro models of ALS, major progress has been made toward gaining insights into the pathobiology of this incurable, fatal disorder. Among these advances is the growing recognition that non-neuronal cells participate in the degeneration of MNs in ALS, which could transform our understanding of the neurobiology of disease and the ability to devise effective disease-modifying therapies. In this review, we examine the contribution of non-cell-autonomous processes to the pathogenesis of ALS, with a focus on glial cells and in particular on astrocytes.
肌萎缩侧索硬化症（ALS）是最常见的成年起病的瘫痪性疾病，主要特征是中枢神经系统中运动神经元（MNs）的丧失。在过去的几十年中，由于在 ALS 的体内和体外模型中进行了深入的研究，人们在了解这种无法治愈的致命疾病的病理生物学方面取得了重大进展。这些进展中包括越来越多的认识，即非神经元细胞参与 ALS 中 MN 的退化，这可能改变我们对疾病神经生物学的理解，并提高设计有效疾病修饰疗法的能力。在这篇综述中，我们研究了非细胞自主过程对 ALS 发病机制的贡献，重点关注神经胶质细胞，特别是星形胶质细胞。
