睡眠碎片化对阿尔茨海默病发病机制的可能影响OA

Sleep fragmentation,characterized by disrupted nocturnal sleep,is a core manifestation of chronic insom-nia and exhibits a close and complex bidirectional relationship with Alzheimer disease(AD).On the one hand,sleep frag-mentation impairs glymphatic system function,reducing the clearance efficiency of toxic metabolites such as amyloid-beta(Aβ)and tau proteins in the brain interstitial fluid,thereby acting as a promoting factor for AD.Concurrently,sleep dis-turbances directly dysregulate pathogenic protein dynamics,and chronic sleep deprivation exacerbates neuroinflammation and oxidative stress,worsening the AD pathological environment.On the other hand,inherent AD pathological changes further aggravate sleep fragmentation.Damage to brain regions associated with AD leads to circadian rhythm disruption and reduced non-rapid eye movement(NREM)sleep.Additionally,imbalances in neurotransmitters such as orexin and melatonin during AD progression contribute to the disintegration of the sleep-wake cycle.This review aims to explore the mutual interactions between sleep fragmentation and AD,identify current research gaps,and provide new directions for fu-ture studies.