Possible Neuropathology of Sleep Disturbance Linking to Alzheimer's Disease: Astrocytic and Microglial Roles

Shu-Yun Xiao; Yi-Jie Liu; Wang Lu; Zhong-Wei Sha; Che Xu; Zhi-Hua Yu; Shin-Da Lee

doi:10.3389/fncel.2022.875138

Possible Neuropathology of Sleep Disturbance Linking to Alzheimer's Disease: Astrocytic and Microglial Roles

Front Cell Neurosci. 2022 Jun 9:16:875138. doi: 10.3389/fncel.2022.875138. eCollection 2022.

Authors

Shu-Yun Xiao¹, Yi-Jie Liu^{2

3}, Wang Lu⁴, Zhong-Wei Sha¹, Che Xu⁵, Zhi-Hua Yu⁶, Shin-Da Lee^{1

7

8}

Affiliations

¹ Department of Mental Diseases, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
² School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
³ Institute of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
⁴ Department of Traditional Treatment, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
⁵ School of Basic Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
⁶ Shanghai Geriatric Institute of Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
⁷ Department of Physical Therapy, Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan.
⁸ Department of Physical Therapy, Asia University, Taichung, Taiwan.

Abstract

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.

Keywords: Alzheimer’s disease; amyloid beta; astrocyte; microglia; sleep disturbance.

Publication types

Review