HIGHLIGHTS
SUMMARY
In sum, sleep loss and proteostasis failure are interactive in AD, involving poor sleep and disrupted circadian rhythmicity which impair biological processes involved in protein clearance. Aβ and tau then feedback to exert direct and indirect effects, via neurodegeneration of sleep-wake controlling neurons, on the sleep-wake cycle. Given the empirical evidence in the recent decade for sleep as a potent regulator of proteostasis, the authors postulate the sleep-proteostasis relationship is critical in the early phase of AD: with Aβ and tau accumulation the neuronal electrophysiological signature of sleep becomes impaired, hence . . .
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