Sleep Deprivation May Be Associated With Alzheimer's

Sleep-deprived mice have higher levels of amyloid-β, greater amyloid-β plaque deposition

05 oct 2009-- Sleep deprivation may play a role in the development of Alzheimer's disease, according to research published online Sept. 24 in Science.

Jae-Eun Kang, Ph.D., of Washington University in St. Louis, and colleagues analyzed data from experiments on mice examining the effects of wakefulness, sleep deprivation, and orexin -- a molecule that regulates wakefulness -- on amyloid-β (Aβ) measurements.

The researchers found that in transgenic and wild-type mice, animals had a difference in interstitial fluid Aβ levels between dark and light phases, with higher levels during the dark period, though fluctuations were linked to the sleep-wake cycle rather than to exposure to light or darkness. Mice subjected to sleep deprivation had significantly higher Aβ levels. Infusion of orexin-A -- which induces rodent wakefulness -- was associated with higher Aβ levels. In addition, mice subjected to sleep restriction for 21 days had higher Aβ plaque deposition; however, chronic orexin receptor blockade for two months decreased Aβ plaque formation in amyloid precursor protein transgenic mice in several brain regions compared to controls.

"Sleep is a complex behavioral state whose ultimate functions remain poorly understood. Sleep disturbances, in addition to being prominent in neurodegenerative diseases, could exacerbate a fundamental process leading to neurodegeneration, and optimization of sleep time could potentially inhibit aggregation of toxic proteins and slow the progression of Alzheimer's disease," the authors conclude.

Abstract
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