A lack of sleep could help toxic plaques develop in the brain, accelerating the progression of Alzheimerās disease.
looked at how sleep affected the levels of beta-amyloid protein in mice and humans. This protein causes plaques to build up in the brain, which some think cause Alzheimerās disease by killing cells.
Holtzmanās group found that beta-amyloid levels were higher in mouse brains when the mice were awake than when they were sleeping.
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Lack of sleep also had an effect on plaque levels: when the mice were sleep-deprived ā forced to stay awake for 20 hours of the day ā they developed more plaques in their brains.
Sleep therapy
Holtzman also tried sending the mice to sleep with a drug that is being trialled for insomnia, called . This reduced the amount of plaque-forming protein.
He suggests that sleeping for longer could limit the formation of plaques, and perhaps block it altogether.
The group also measured levels of beta-amyloid in the cerebrospinal fluid of 10 healthy men, both at night and during the day. Levels were lower at night, suggesting that sleep might also help keep levels of the plaque protein low in humans.
Holtzman reckons that when weāre awake, our brains are more active, and that this may cause us to produce more beta-amyloid protein.
Pills arenāt the answer
Neuroscientist of the University of Cambridge says that people with Alzheimerās are known to suffer sleep abnormalities, but that whether these are a cause or a symptom of the disease is unknown.
He says the new results are interesting, but cautions against encouraging people with Alzheimerās to take sleeping pills in the hope that sleep will mitigate the disease. Instead, he suggests exercise to induce sleep might be a good idea if later studies confirm a link between sleep and Alzheimerās progression.
āIt is interesting that there may be a link between sleep and the build-up of the protein associated with the development of Alzheimerās disease,ā says Clive Ballard, director of research at the in London. āHowever, there are many other biological factors that may have an impact on the proteinās production, so further research in this area would be needed.ā
Recently, for example, several drugs that clear plaques failed to relieve the symptoms of Alzheimerās. And earlier this month, two studies suggested that disruptions of the immune system, the way cells metabolise fat and wear and tear on the circulatory system may be as much to blame for Alzheimerās as plaques.
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