阿尔茨海默病(Alzheimer's disease,AD)是常见的神经变性病,以进行性记忆丧失和认知能力缺陷为特征.AD的病理特征是细胞外β淀粉样蛋白(β-amyloid protein,Aβ)沉积和细胞内Tau蛋白累积.AD患者具有较高的睡眠障碍发生率,而睡眠剥夺(sleep deprivation,SD)是AD发生和进展的重要危险因素.SD损害认知功能并加速AD病理学进展.SD可以增加小鼠体内Aβ沉积的发生风险,也会进一步导致AD患者的认知功能障碍;SD可以增加Aβ和Tau蛋白的沉积,诱导细胞自噬体、溶酶体途径的功能障碍和细胞过度自噬,激活小胶质细胞导致神经炎症发生,降低细胞过氧化系统而使脂质过氧化增加,具有抑制类淋巴系统清除脑中的代谢废物的功能,从而加速AD的进展.SD在AD中的作用机制和二者之间的关系具有重要的临床意义,可为探索新的AD干预策略提供理论依据.
Alzheimer's disease(AD)is a common neurodegenerative disease characterized by cognitive decline and dysfunction in the nervous system.The neuropathology features of AD include the deposition of extracellular β-amyloid protein(Aβ)and the accumulation of intracellular Tau protein.AD Patients have a higher prevalence of sleep disorders,and sleep deprivation(SD)is considered an important risk factor for the occurrence and progression of AD.SD impairs cognitive function and accelerates the pathological progression of AD.It increases the risk of Aβ deposition in mice and further leads to cognitive dysfunction in AD patients.SD can enhance the deposition of Aβ and Tau proteins,induce dysfunction in cellular autophagy and lysosomal pathway,activate microglia leading to neuroinflammation,decrease the efficiency of the cell's oxidative system,increase lipid peroxidation,and inhibit the clearance of metabolic waste from the brain through the glymphatic system,thereby accelerating the progression of AD.The mechanism of SD in AD and the relationship between the two have important clinical significance,providing a theoretical basis for exploring new AD intervention strategies.