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

Music Gene

A Genetic Basis for Music?
A QUANTUM OF SCIENCE

Musical legacy found in a gene associated with social interaction traits – including love

Researchers in Finland recently reported a study in which 19 Finnish familes (343 individuals) with many professional or active amateur musicians among them were studied for genetic similarities. The study found that a single gene, AVPR1A (for arginine vasopressin receptor 1A), held a strong statistical correlation to creative musical abilities such as pitch, tempo and composition, especially when members of multiple generations all shared musical ability. So what is arginine vasopressin?

Peptide hormones, of which the vasopressins are a subfamily, are composed of short cyclic chains of amino acids (nine, in this case) and regulate a number of physiological functions. Arginine vasopression (abbreviated AVP) controls hydration through kidney function, including the stimulation of urine dilution and concentration in balance with the body’s need for extra water. For this activity it is secreted into the bloodstream, but some AVP is also found in the brain, where it binds to a specialized receptor – the one encoded by the gene AVPR1A. Binding of AVP to AVPR1A stimulates the brain to release neurotransmitters that play into "social behavior" responses, including the mate bonding behavior found in voles and, to a greater or lesser extent, in humans. Some studies have even suggested that these same neurotransmitters play a role in feelings of altruism, or love.

Is there a single gene that determines who is musical and who is not? These findings are preliminary and far from exhaustive, but they point to a biological function encouraging the spread and preservation of the AVPR1A gene. If, as suggested, the AVP/AVPR1A peptide hormone receptor plays a role in social behavior and other emotional attachment activities in higher mammals, it could easily be linked to the development of early human societies via the universal language: music.

For more information:

Original PLOS article


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