"Elite sleeper” gene study offers hope for novel dementia treatment
Are you one of those lucky people who seem to be able to thrive on between four and six hours of sleep per night? You may be what UC San Francisco researchers have dubbed an “elite sleeper,” and a new study reports the same genes associated with healthy short sleep patterns may also slow the onset of neurodegenerative diseases such as Alzheimer’s.
In 2018, the world’s largest sleep study concluded between seven and eight hours of sleep each night is the sweet spot to maintain optimal cognitive performance and general health. For most people, sleeping less than six hours a night can lead to a number of deleterious health outcomes, from increased dementia risk in later life to higher chances of early death.
But some people can comfortably sleep just a few hours a night while maintaining good health, and researchers have been closely studying these “elite sleepers." More than a decade ago UC San Francisco scientists discovered the first gene associated with these rare short sleep behaviors. Since then, the team has found five genes they believe are linked to a condition now named Familial Natural Short Sleep (FNSS).
“There’s a dogma in the field that everyone needs eight hours of sleep, but our work to date confirms that the amount of sleep people need differs based on genetics,” explained co-senior author Louis Ptacek. “Think of it as analogous to height; there’s no perfect amount of height, each person is different. We’ve shown that the case is similar for sleep.”
The new study set out to investigate whether these short sleep gene variants directly protect against neurodegeneration linked to Alzheimer’s. To do this the researchers focused on two specific gene variants previously linked to FNSS and several mouse models genetically engineered to be susceptible to the development of Alzheimer’s.
Across several animal experiments the researchers demonstrated both FNSS gene variants slowed the progression of Alzheimer’s pathology in the mice. The mechanisms by which the gene variants protect from neurodegeneration are still unclear but the researchers do indicate the findings affirm genetic factors do play a role in slowing the progression of Alzheimer’s pathology.
The researchers also hypothesize the genes linked to FNSS likely make the process of sleep more efficient. This means those carrying these particular variants seem to accomplish all the brain benefits of longer sleep in shorter periods of time to normal people.
Co-senior author Ying-Hui Fu said the findings fit with plenty of observational research associating poor sleep and brain disease.
“Sleep problems are common in all diseases of the brain,” said Fu. “This makes sense because sleep is a complex activity. 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.”
It is very early days but the researchers argue the implications of these genetic sleep studies could be significant. Linking these specific gene variants to healthy sleep behaviors can point scientists in novel directions for new kinds of treatments targeting a variety of brain diseases. Drugs that influence the expression of these short sleep genes could hypothetically be developed to enhance the quality of sleep in older adults and ultimately prevent or slow the onset of neurodegenerative disease.
“This work opens the door to a new understanding of how to delay and possibly prevent a lot of diseases,” added Fu. “Our goal really is to help everyone live healthier and longer through getting optimum sleep.”
The new study was published in the journal iScience.