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Updated: Aug 13, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Beyond the sleep-amyloid interactions in Alzheimer's disease pathogenesis
Shen Ning1,2, Mehdi Jorfi1,3
1Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts.
Abstract:
Cognitive impairment in older adults is associated with sleep and circadian rhythm disturbances. Numerous studies have linked disrupted sleep and circadian rhythms with amyloid-β (Aβ), a key pathological hallmark in Alzheimer's disease (AD). While previous evidence suggests that Aβ initiates AD pathogenesis, tau, another major hallmark of AD, seems to drive neurodegeneration. Recent studies imply that sleep-wake cycles affect brain tau more significantly than Aβ levels, leading to accelerated AD progression and cognitive decline. The study of sleep disturbances in AD is shedding light on our understanding of the mechanism underlying sleep disturbances in AD and dementia.
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