Sleep Architecture Disruption as a Predictor of Cognitive Decline in Parkinson's Disease

Abstract

Cognitive decline is one of the most consequential non-motor complications of Parkinson's disease (PD), but at diagnosis motor features give little indication of who will progress to mild cognitive impairment or dementia. This short communication synthesizes recent evidence that disrupted sleep architecture is not merely a common accompaniment of PD but a measurable, mechanistically plausible predictor of cognitive trajectory. We trace two converging lines of evidence: reduced slow-wave sleep and frontal EEG delta power are associated with poorer global cognition and executive function in PD, plausibly through impaired glymphatic clearance of misfolded proteins during deep sleep; and REM sleep behavior disorder, a loss of normal REM muscle atonia, is among the strongest known prodromal markers of neurodegeneration, with a large multicentre cohort reporting roughly 6% annual phenoconversion to parkinsonism or dementia. Newer biomarkers, including neurofilament light chain, cardiac MIBG uptake, and quantitative scoring of REM sleep without atonia, are beginning to refine this prediction further, while depression appears to mediate part of the sleep-cognition association. We close by noting that whether treating sleep architecture disruption, through dopaminergic optimization, circadian interventions, or treatment of comorbid sleep apnea, can slow cognitive decline rather than simply improving sleep quality remains an open and clinically important question.