Chronic Sleep Restriction as a Modifiable Risk Factor for Alzheimer’s Disease: A Narrative Review on Hippocampal Memory Consolidation, Amyloid-β Pathology, and Epidemiological Evidence

Abstract

Chronic sleep restriction has become increasingly prevalent and has emerged as a potentially modifiable factor associated with cognitive decline and Alzheimer’s disease (AD). This narrative review synthesized current neuroscientific, clinical, and epidemiological evidence examining the relationship between habitual sleep durations of seven hours per night, hippocampal memory consolidation, AD-related neuropathology, and dementia risk. Literature published between 2015 and June 2026 was identified through searches of PubMed/MEDLINE, Scopus, and Web of Science. The reviewed evidence indicates that insufficient sleep is associated with impaired glymphatic clearance, amyloid-β accumulation, tau pathology, oxidative stress, neuroinflammation, mitochondrial dysfunction, synaptic dysfunction, and deficits in hippocampal-dependent memory. Epidemiological studies further report associations between habitual short sleep duration and increased risks of cognitive decline and dementia. Although much of the mechanistic evidence originates from animal models and current human studies remain insufficient to establish causality, the convergence of experimental and epidemiological findings supports the biological plausibility of chronic sleep restriction as a contributor to processes implicated in Alzheimer's disease. These findings highlight sleep health as an underrecognized consideration in dementia prevention and identify important priorities for future longitudinal and interventional research.