Alzheimer's disease is a neurological condition where patients experience difficulty sleeping. However, new research indicates that poor sleeping habits may be a risk factor for developing Alzheimer's disease.
Researchers at Washington University in St. Louis investigated the effects of decreased sleep on plaque formation. The Alzheimer's Association states that “plaques build up between [the] nerve cells. They contain deposits of a protein fragment called beta-amyloids.” The plaques are abnormalities that only appear in Alzheimer's disease brains, where they damage and kill nerve cells. Using microdialysis to measure protein levels, researchers tested mice who were sleep deprived and mice with normal sleeping hours.
The beta-amyloid levels in the brain tissue did not change in the mice; however, the levels of beta-amyloid released into the brain fluid varied throughout the day. Researchers found that the amount of beta-amyloid in the brain fluid was associated with the time of day. As a result, mice who were sleep deprived had an increase of beta-amyloid in their brain fluid.
Another factor in the beta-amyloid increase was the hormone orexin, which promotes wakefulness. When the mice were injected with orexin, the researchers found that the mice had an increase of beta-amyloid in the brain fluid. If a drug that blocked the effects of orexin was used, the amount of beta-amyloid was decreased. Sleep-deprived mice were monitored for three weeks; during this time, the mice had a greater plaque build up when compared to normal mice. However, introduction of an anti-orexin drug stopped the buildup.
In the second stage of the study, researchers also tested the cerebrospinal fluid of healthy adults. A similar effect was also found in humans: participants who were not getting enough sleep had an increased level of beta-amyloid. The researchers suggest that the connection between the lack of sleep and the increase in beta-amyloid is the most serious for people in their 50s; around this time plaques begin to form, so the decreased sleep could speed up the production.
However, while the anti-orexin injection prevented the progression of beta-amyloid formation, it might not be a plausible as a treatment. Masashi Yanagisawa of the University of Texas Southwestern Medical Center was quoted in the US News and World Reports article as saying “treating patients chronically with orexin inhibitors is really not an option.” The article explains that unless the orexin inhibiting drug was given in small doses, it would cause sleepiness.
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Elizabeth Stannard Gromisch received her bachelor’s of science degree in neuroscience from Trinity College in Hartford, CT in May 2009. She is the Hartford Women's Health Examiner and she writes about abuse on Suite 101.