Sleep delays Alzheimer’s?

A QUANTUM OF SCIENCE

Sleep-cycle neurotransmitters correlate with concentration of Alzheimer’s-causing protein

Alzheimer’s Disease (AD) is a form of late-adulthood dementia caused by brain matter deterioration. This process is associated with the accumulation of a protein called beta-amyloid. When functioning normally, beta-amyloid proteins are soluble and circulate throughout the brain institial fluid; but sometimes their concentration rises to the point where the amyloid protein precipitates, forming insoluble plaques in the brain that lead to necrosis and loss of neuronal function – the classic Alzheimer’s symptoms. But what causes beta-amyloid concentrations to rise to the point where they begin to accumulate as brain-killing plaques?

While the root cause is still unknown, scientists at Washington University in St. Louis have found an unprecedented correlation between beta-amyloid concentration and sleep. Using mice, this study followed beta-amyloid concentrations in brain fluid over the course of multiple sleep cycles. Their findings, just published in the journal Science, show that beta-amyloid concentrations in the brain fell sharply during sleep, only to rise against during waking hours. In additional experiments, researchers showed that sleep deprivation (with or without orexin, a neurochemical that promotes wakefulness) also artificially maintained a high concentration of beta-amyloid, while a chemical that prevents orexin from binding to brain receptors artificially decreased beta-amyloid concentrations.

While the causes of this association are not yet clear, the study points to a potent and previously unknown link between sleep and the pathogenesis of Alzheimer’s disease.

For more information:



Amyloid-Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle (Kang et al)

Beta-amyloid protein (Wikipedia)

Alzheimer’s Disease (Wikipedia)


© AQOS / P. Smalley (2009)
Reproduction with attribution is appreciation