Beyond the sleep-amyloid interactions in Alzheimer’s disease pathogenesis

Author:

Ning Shen12,Jorfi Mehdi13ORCID

Affiliation:

1. Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts

2. Graduate Program for Neuroscience, Boston University School of Medicine, Boston, Massachusetts

3. Center for Engineering in Medicine, Department of Surgery, 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.

Funder

Boston University School of Medicine MD/PhD Dean's Scholarship

Cure Alzheimer's Fund (CAF)

Publisher

American Physiological Society

Subject

Physiology,General Neuroscience

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