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Sleep disruption is intrinsically linked with Alzheimer’s disease and its pathophysiology, with characteristic changes in sleep emerging early in life, well before the clinical onset of the disease. A key player in the development of Alzheimer’s disease is amyloid-beta. Insufficient sleep increases the production of amyloid-beta, and amyloid-beta deposition, in turn, impairs sleep in a vicious, self-perpetuating loop. Findings from a new study demonstrate that sleep deprivation also increases blood levels of tau, a protein found in the brain.
Tau is a microtubule-bound protein that forms the neurofibrillary “tau tangles” associated with Alzheimer’s disease. Tau tangles disrupt the transport of metabolites, lipids, and mitochondria across a neuron to the synapse where neurotransmission occurs. Diminished slow-wave sleep is associated with higher levels of tau in the brain. Elevated tau is a sign of Alzheimer’s disease and has been linked to cognitive decline.
The two-condition crossover study involved 15 healthy young men who were randomized to regimens of either two nights of consecutive sleep or one night of sleep followed by one night of sleep deprivation. Following the one night of sleep deprivation, participants' blood levels of tau increased approximately 17 percent, compared to an approximately 2 percent increase following the night of sleep. Other biomarkers of Alzheimer’s disease-associated proteins were unchanged. While tau tangle formation in neurons can disrupt normal function, it is unclear what elevated blood levels of tau protein mean. Future studies are needed to elucidate this finding.
Watch this clip featuring Dr. Matthew Walker in which he describes current research focused on identifying age-related sleep deprivation vulnerability windows for prevention of Alzheimer’s disease.