Chronic sleep loss is a risk factor for Alzheimer's disease (AD), and reduced and fragmented sleep is increasingly appreciated as an early-onset diagnostic and potential therapeutic target for AD. However, robustly modeling AD-like sleep deficits in fruit flies has often been challenging. We report that cold-raising unmasks deficits in sleep duration, fragmentation, and latency in one such model pan-neuronally expressing a highly pathogenic AD-associated amyloid species. This sensitized model provides a promising platform for identifying potential metabolic, proteostatic, glymphatic, and other candidate mediators bidirectionally linking sleep and AD.
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