Summary: Researchers have identified five genes across the genome that enable efficient sleep.
Source: UCSF
Researchers at the University of California, San Francisco report that some individuals carry genetic variants that allow them to sleep fewer hours while maintaining alertness and cognitive function. These “elite sleepers” can thrive on approximately four to six hours of sleep per night, and their genetic profile appears linked to psychological resilience and reduced vulnerability to certain neurodegenerative processes.
“A long-standing belief in sleep research is that everyone needs eight hours of sleep,” said neurologist Louis Ptacek, MD, a senior author on the study published in iScience on March 15, 2022. “Our findings show that sleep need varies by genetics. Just as height differs among people, so does the ideal amount of sleep.”
For more than ten years, Ptacek and co-senior author Ying-Hui Fu, PhD, both members of the UCSF Weill Institute for Neurosciences, have studied families with Familial Natural Short Sleep (FNSS)—a hereditary trait in which people prefer and function well on a shorter sleep window. The team has so far identified five genes across the genome that contribute to this efficient sleep phenotype, and they emphasize that additional FNSS genes remain to be discovered.
In this study, Fu tested the hypothesis that genetic short sleepers might be partially protected from neurodegenerative disease. This idea differs from the common view that insufficient sleep accelerates neurodegeneration; the researchers propose that when sleep is more efficient, shorter duration does not necessarily mean inadequate sleep. In other words, if essential restorative processes are completed in less time, the brain may still receive the benefits it needs.
To explore this concept, the researchers studied mouse models of Alzheimer’s disease, a condition they selected because of its prevalence and the strong need to understand modifiable factors. They bred mice carrying an FNSS-associated gene together with genes that increase Alzheimer’s risk. These double-mutant mice developed far fewer of the protein aggregates that are hallmarks of dementia. The experiment was repeated using a different short-sleep gene and a separate Alzheimer-related gene, producing similar reductions in pathological aggregates.
Based on these results, Fu and Ptacek anticipate that efficient-sleep genes could offer comparable protection across a range of brain disorders. They suggest that improving sleep quality and efficiency might delay disease progression in multiple neurological conditions, because disrupted sleep is a common symptom across many brain illnesses.
“Sleep disturbances occur in virtually all brain diseases,” Fu said. “Sleep is a complex, coordinated activity that depends on many brain regions working together. When those regions are damaged, it becomes harder to fall asleep and to achieve restorative sleep.”
Understanding the biological mechanisms that regulate sleep could point to drug targets and therapeutic strategies to prevent or treat sleep disorders and potentially slow neurodegenerative processes. The researchers compare the search for all contributing genes to assembling a large jigsaw puzzle: each mutation or variant they discover is a new piece that helps clarify the overall picture.
“Every mutation we find is another piece,” Ptacek said. “Right now we’re working on the edges and corners so we can begin to connect pieces and reveal the full image.”
Although identifying the many genes involved will take time, some of the genes already discovered are promising because they map to pathways that can be influenced by existing drugs. The team hopes that, within the next decade, these insights will contribute to new treatments that help people with brain disorders obtain better, more restorative sleep and thereby improve health outcomes and quality of life.
“This research opens a path to better understand how to delay or possibly prevent a range of diseases,” Fu said. “Our ultimate goal is to help people live healthier, longer lives by achieving optimal sleep.”
Authors: Additional authors on the study include Qing Dong, Nicholas W. Gentry, Thomas McMahon, Maya Yamazaki, Lorena Benitez-Rivera, and Tammy Wang, all of UCSF, and Li Gan of Weill Cornell Medicine.
Funding: This work was supported by NIH grants NS117929, NS072360 and NS104782 and the William Bowes Neurogenetics Fund.
About this sleep and genetics research news
Author: Robin Marks
Source: UCSF
Contact: Robin Marks – UCSF
Image: The image is in the public domain
Original Research: The findings will appear in iScience