Henstridge Christopher M, Tzioras Makis, Paolicelli Rosa C
Centre for Discovery Brain Sciences, The University of Edinburgh, Edinburgh, United Kingdom.
Dementia Research Institute UK, The University of Edinburgh, Edinburgh, United Kingdom.
Front Cell Neurosci. 2019 Feb 26;13:63. doi: 10.3389/fncel.2019.00063. eCollection 2019.
Synapse loss is an early feature shared by many neurodegenerative diseases, and it represents the major correlate of cognitive impairment. Recent studies reveal that microglia and astrocytes play a major role in synapse elimination, contributing to network dysfunction associated with neurodegeneration. Excitatory and inhibitory activity can be affected by glia-mediated synapse loss, resulting in imbalanced synaptic transmission and subsequent synaptic dysfunction. Here, we review the recent literature on the contribution of glia to excitatory/inhibitory imbalance, in the context of the most common neurodegenerative disorders. A better understanding of the mechanisms underlying pathological synapse loss will be instrumental to design targeted therapeutic interventions, taking in account the emerging roles of microglia and astrocytes in synapse remodeling.
突触丢失是许多神经退行性疾病共有的早期特征，也是认知障碍的主要相关因素。最近的研究表明，小胶质细胞和星形胶质细胞在突触消除中起主要作用，导致与神经退行性变相关的网络功能障碍。兴奋性和抑制性活动会受到胶质细胞介导的突触丢失的影响，导致突触传递失衡及随后的突触功能障碍。在此，我们在最常见的神经退行性疾病背景下，综述了关于胶质细胞对兴奋性/抑制性失衡作用的最新文献。更好地理解病理性突触丢失的潜在机制，将有助于设计有针对性的治疗干预措施，同时考虑到小胶质细胞和星形胶质细胞在突触重塑中的新作用。
