Xiao Shu-Yun, Liu Yi-Jie, Lu Wang, Sha Zhong-Wei, Xu Che, Yu Zhi-Hua, Lee Shin-Da
Department of Mental Diseases, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Front Cell Neurosci. 2022 Jun 9;16:875138. doi: 10.3389/fncel.2022.875138. eCollection 2022.
Sleep disturbances not only deteriorate Alzheimer's disease (AD) progress by affecting cognitive states but also accelerate the neuropathological changes of AD. Astrocytes and microglia are the principal players in the regulation of both sleep and AD. We proposed that possible astrocyte-mediated and microglia-mediated neuropathological changes of sleep disturbances linked to AD, such as astrocytic adenosinergic A1, A2, and A3 regulation; astrocytic dopamine and serotonin; astrocyte-mediated proinflammatory status (TNFα); sleep disturbance-attenuated microglial CX3CR1 and P2Y12; microglial Iba-1 and astrocytic glial fibrillary acidic protein (GFAP); and microglia-mediated proinflammatory status (IL-1b, IL-6, IL-10, and TNFα). Furthermore, astrocytic and microglial amyloid beta (Aβ) and tau in AD were reviewed, such as astrocytic Aβ interaction in AD; astrocyte-mediated proinflammation in AD; astrocytic interaction with Aβ in the central nervous system (CNS); astrocytic apolipoprotein E (ApoE)-induced Aβ clearance in AD, as well as microglial Aβ clearance and aggregation in AD; proinflammation-induced microglial Aβ aggregation in AD; microglial-accumulated tau in AD; and microglial ApoE and TREM2 in AD. We reviewed astrocytic and microglial roles in AD and sleep, such as astrocyte/microglial-mediated proinflammation in AD and sleep; astrocytic ApoE in sleep and AD; and accumulated Aβ-triggered synaptic abnormalities in sleep disturbance. This review will provide a possible astrocytic and microglial mechanism of sleep disturbance linked to AD.
睡眠障碍不仅会通过影响认知状态而使阿尔茨海默病（AD）的病情恶化，还会加速AD的神经病理变化。星形胶质细胞和小胶质细胞是睡眠和AD调节过程中的主要参与者。我们提出，睡眠障碍可能通过星形胶质细胞和小胶质细胞介导与AD相关的神经病理变化，例如星形胶质细胞腺苷能A1、A2和A3调节；星形胶质细胞多巴胺和5-羟色胺；星形胶质细胞介导的促炎状态（肿瘤坏死因子α）；睡眠障碍减弱的小胶质细胞CX3CR1和P2Y12；小胶质细胞离子钙结合衔接分子1和星形胶质细胞胶质纤维酸性蛋白（GFAP）；以及小胶质细胞介导的促炎状态（白细胞介素-1β、白细胞介素-6、白细胞介素-10和肿瘤坏死因子α）。此外，还综述了AD中星形胶质细胞和小胶质细胞的β淀粉样蛋白（Aβ）及tau蛋白，例如AD中星形胶质细胞Aβ相互作用；AD中星形胶质细胞介导的促炎作用；中枢神经系统（CNS）中星形胶质细胞与Aβ的相互作用；AD中星形胶质细胞载脂蛋白E（ApoE）诱导的Aβ清除，以及AD中小胶质细胞Aβ清除和聚集；AD中促炎诱导的小胶质细胞Aβ聚集；AD中小胶质细胞积累的tau蛋白；以及AD中小胶质细胞ApoE和触发受体表达于髓样细胞2（TREM2）。我们综述了星形胶质细胞和小胶质细胞在AD和睡眠中的作用，例如AD和睡眠中星形胶质细胞/小胶质细胞介导的促炎作用；睡眠和AD中的星形胶质细胞ApoE；以及睡眠障碍中Aβ积累引发的突触异常。本综述将提供睡眠障碍与AD相关的一种可能的星形胶质细胞和小胶质细胞机制。
