Department of Biotechnology, Guru Nanak Dev University, Amritsar, Punjab, 143005, India.
Department of Dermatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Neurochem Res. 2022 Jul;47(7):1799-1815. doi: 10.1007/s11064-022-03578-0. Epub 2022 Mar 18.
Poor quality and quantity of sleep are very common in elderly people throughout the world. Growing evidence has suggested that sleep disturbances could accelerate the process of neurodegeneration. Recent reports have shown a positive correlation between sleep deprivation and amyloid-β (Aβ)/tau aggregation in the brain of Alzheimer's patients. Glial cells have long been implicated in the progression of Alzheimer's disease (AD) and recent findings have also suggested their role in regulating sleep homeostasis. However, how glial cells control the sleep-wake balance and exactly how disturbed sleep may act as a trigger for Alzheimer's or other neurological disorders have recently gotten attention. In an attempt to connect the dots, the present review has highlighted the role of glia-derived sleep regulatory molecules in AD pathogenesis. Role of glia in sleep disturbance and Alzheimer's progression.
全世界的老年人普遍存在睡眠质量和数量差的问题。越来越多的证据表明,睡眠障碍可能会加速神经退行性变的进程。最近的报告显示,睡眠剥夺与阿尔茨海默病患者大脑中的淀粉样蛋白-β (Aβ)/tau 聚集之间存在正相关关系。神经胶质细胞长期以来一直被认为与阿尔茨海默病 (AD) 的进展有关,最近的研究结果还表明它们在调节睡眠稳态中的作用。然而,神经胶质细胞如何控制睡眠-觉醒平衡,以及睡眠障碍如何成为阿尔茨海默病或其他神经退行性疾病的诱因,最近引起了人们的关注。为了将这些线索联系起来,本综述强调了神经胶质细胞衍生的睡眠调节分子在 AD 发病机制中的作用。神经胶质细胞在睡眠障碍和阿尔茨海默病进展中的作用。