Want to Ward Off Alzheimer's? Get Your ZZZZZZZZs.
The definition of Alzheimer's disease (AD) depends on whom you ask. The disorder than manifests itself as confusion and forgetfulness in a patient is--to the neuroscientist--a buildup of tangles and plaques in the brain. The plaques are accumulations of an amyloid protein in the spaces between brain cells. Nerve cells produce the protein and secrete it into the fluid that fills the spaces. The protein is soluble in small amounts, but as its concentration increases, so does the chance that it will condense into plaques. Presumably, the larger the number of plaques, the greater the severity of the disease.
Neuroscientists want to know what factors regulate the release of soluble amyloid protein and its subsequent buildup in the brain. In a recent study, a research team at Washington University-St. Louis and Stanford University studied the brains of mice. The team found that amyloid levels varied during the 24-hour sleep-wake cycle. The longer the mice stayed awake, the higher their amyloid levels rose. Similarly, the longer the mice slept, the lower their levels fell.
Some of the mice in the study were genetically engineered to express a human form of the amyloid protein. The researchers subjected the animals to periods of sleep deprivation. The mice stayed awake for 20 hours a day for three weeks. The sleep-deprived mice secreted more amyloid, and their brains formed plaques at a greater rate than that measured in their normal-sleeping littermates.
Do sleep-wake changes in amyloid protein occur in humans as they do in mice? Apparently so. The researchers measured amyloid levels in the cerebrospinal fluid of 10 young healthy male volunteers over a 33- hour period. The scientists found the same waking-sleeping variation in the men that they found in the mice. Amyloid levels rose the longer the men stayed awake; amyloid levels fell when the men slept.
The conclusion is obvious. "Optimization of sleep time could potentially inhibit aggregation of toxic proteins and slow the progression of AD," the researchers say.
References:
Jae-Eun Kang, Miranda M. Lim, Randall J. Bateman, James J. Lee, Liam P. Smyth, John R. Cirrito, Nobuhiro Fujiki, Seiji Nishino, and David M. Holtzman. "Amyloid-β Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle," Science Published online September 24, 2009.
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