Purpose of review: The escalating global burden of neurodegenerative diseases, coupled with a lack of disease-modifying therapies, has intensified the search for modifiable risk factors. This review aims to synthesize the extensive recent literature to position the brain's waste clearance pathway, the glymphatic system, as a core physiological bridge connecting disordered sleep to the molecular pathogenesis of neurodegeneration, thereby providing a coherent mechanistic framework for clinicians and researchers.
Recent findings: Compelling evidence from the last decade solidifies the glymphatic system's dependence on deep, non-rapid eye movement (NREM) sleep for the efficient clearance of neurotoxic metabolic byproducts, including amyloid-beta (Aβ), tau, and α-synuclein. Common and highly prevalent clinical conditions, including obstructive sleep apnea (OSA), chronic insomnia, and circadian rhythm disorders, have been shown to fundamentally disrupt this vital clearance process. The pathogenic drivers are multifactorial, involving sleep fragmentation-induced sympathetic hyperactivity, intermittent hypoxia-driven vascular damage, and neuroinflammatory activation. Glymphatic impairment is a key, non-redundant pathophysiological mediator between sleep disorders and the initiation and propagation of neurodegenerative cascades. This understanding elevates the status of sleep from a passive correlate to an active, modifiable factor in brain health. Consequently, the systematic diagnosis and effective management of sleep disorders emerge as tangible, accessible, and powerful strategies for primary and secondary neuroprotection.
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