Genetic mutations that cause shorter sleeping times have been shown to reduce neuropathology in mouse models of Alzheimer's disease (AD), indicating that more efficient sleep may protect against neurodegenerative diseases.
The quality and length of sleep is important for protecting against cognitive decline. Sleep has been linked to neurodegeneration during AD, with disrupted sleep patterns correlated with decreased cognition and faster disease progression. In a new study published in iScience, researchers aimed to further understand the connection between sleep and AD pathology.
Professor Ying-Hui Fu, senior author of the study at University of California, San Francisco said: 'Sleep problems are common in all diseases of the brain… Many parts of your brain have to work together for you to fall asleep and to wake up. When these parts of the brain are damaged, it makes it harder to sleep or get quality sleep.'
Professor Fu, and co-senior author on the study Professor Louis Ptacek, have spent years studying mutations in what they call 'elite sleeper' genes which cause Familial Natural Short Sleep (FNSS). People with these mutations sleep fewer hours than normal, requiring only four to six hours per night in adulthood. The researchers believe these mutations enhance sleep efficiency, meaning only a short amount of sleep is needed for the brain to get its necessary benefits. Interestingly, when FNSS mutation carriers reach the age when AD is likely to develop, they still maintain normal cognitive abilities. Yet, it was unknown how these 'elite sleeper' genes protect against neurodegeneration.
In the study, researchers investigated how the changed sleep caused by FNSS mutations related to AD pathology by crossing mouse models containing FNSS mutations with two mouse models which develop a key aspect of AD pathology: toxic build-ups of proteins in the brain called amyloid-beta and tau. The amount of these protein aggregates in the brain was compared between the AD mice with the FNSS mutations and the AD mice without the mutations. Intriguingly, mice with the FNSS mutations had less AD pathology than the mouse models without the mutations, demonstrating that the mutations protected the mice from neurodegeneration.
The study findings suggest that improving sleep may have potential as a therapeutic target for delaying disease progression in AD. Furthermore, the study paves the way for similar investigations into the effect of these elite sleeper genes on other brain conditions; improving sleep efficiency may protect against a whole spectrum of diseases. As Professor Ptacek said: 'This work opens the door to a new understanding of how to delay and possibly prevent a lot of diseases. Our goal really is to help everyone live healthier and longer through getting optimum sleep.'
Sources and References
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Familial natural short sleep mutations reduce Alzheimer pathology in mice
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When it comes to sleep, it's quality over quantity
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Elite sleepers' can survive on less than six hours without raised dementia risk
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Long naps may be early sign of Alzheimer's disease, study shows
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Elite sleeper' gene study offers hope for novel dementia treatment
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Excessive napping could be a sign of dementia, study finds
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Excessive napping and Alzheimer's linked in study
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