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

Newest Alzheimer's Drug: Coffee?

A QUANTUM OF SCIENCE

New research suggests caffeine may not only protect but can also reverse Alzheimer's Disease symptoms

Today's issue of the Journal of Alzheimer's Disease contains two reports involving the effects of caffeine on mice bred to mimic the biochemical degeneration of cognition found in human Alzheimer's disease. Briefly, the major source of this neural degeneration is the accumulation of a protein called Amyloid-β (or Aβ). A natural protein, Aβ can sometimes mis-fold and in that state becomes impervious to the normal cellular processes that break down aging proteins for recycling. Because it cannot be broken down, mis-folded Aβ accumulates and eventually causes cell death in the tissues surrounding it. Alzheimer's disease results when this takes place in brain tissue.

Researchers are interested in the process by which Aβ mis-folds, accumulates and - just possibly - might be eradicated. In the studies published today in the Journal of Alzheimer's Disease, researchers found that caffeine can not only protect Alzheimer's-prone mice from the accumulation of Aβ, but can even reduce Aβ levels in the brains and blood of mice who already have advanced Alzheimer's conditions. This is not the first report of caffeine's effects, but the two studies are back-to-back illustrations of the growing body of evidence linking caffeine to treatment for Alzheimer's even after the condition is diagnosed. Additionally, the levels of caffeine used in this study are relevant - the equivalent of about five cups of coffee per day for a human. This is exciting as it suggests that caffeine treatment might be possible without resorting to levels so high as to cause dangerous side-effects to humans.

For more information:

Caffeine Reverses Cognitive Impairment and Decreases Brain Amyloid-β Levels in Aged Alzheimer’s Disease Mice (Arendash et al)

Caffeine Suppresses Amyloid-β Levels in Plasma and Brain of Alzheimer’s Disease Transgenic Mice (Chuanhai et al)

© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation!