Virtually all medical associations across the world recommend you get at least seven hours of sleep per night, ideally eight. But that’s just a guideline. Some people feel fully rested after just six or even four hours of sleep. According to a new study from the University of California San Francisco, these short sleepers are blessed with a number of genes that efficiently rejuvenate the body and brain in a shorter time window than most people require.

People who are able to function fully on four to six hours of sleep have what scientists call Familial Natural Short Sleep (FNSS). Louis Ptacek, a professor of neurology at the University of California San Francisco and lead author of the new study, has been studying people with FNSS for over a decade. Previous studies showed that FNSS runs in the family. Five genes have been identified thus far linked to FNSS.

Ptacek’s research also suggests that people with FNSS, which he calls ‘elite sleepers’, have above-average psychological resilience and resistance to neurodegenerative diseases like Alzheimer’s. That’s particularly striking because Alzheimer’s has been linked to not getting enough sleep. But if these elite sleepers are any indication, sleep quality seems to be much more important than sleep quantity.

In a new study, Ptacek’s team investigated the link between Alzheimer’s and short sleep in detail. The researchers bred mice that had both FNSS genes and genes that are known to predispose them to Alzheimer’s. These mice ended up developing fewer plaques (abnormal clusters of protein fragments that build up between nerve cells) and tangles (made up of twisted strands of another protein), both considered hallmark aggregates of Alzheimer’s disease (AD). Similar results were obtained when the experiment was repeated with mice that had a different short-sleep gene.

“AD is the leading cause of age-related neurodegeneration, accounting for nearly 75% of all dementia cases. AD is incredibly complex, and its etiology is characterized by the interplay between many physiological, genetic, and environmental influences. Great effort has been put forward during the last few decades in seeking cures for AD, yet most of this has focused on deleterious genetic influences over preventive ones. FNSS individuals do not appear to suffer from increased risk of dementia despite lifelong shorter sleep duration, implying a potential protective effect stemming from these mutations,” the authors wrote in the journal Science.

Sleep problems are a common hallmark of brain diseases. “This makes sense because sleep is a complex activity. Many parts of your brain have to work together for you to fall asleep and wake up. When these parts of the brain are damaged, it makes it harder to sleep or get quality sleep,” Ptacek said, adding that this makes understanding the biological underpinnings of sleep regulation all the more important.

The few genes Ptacek and colleagues have identified thus far could be targeted by drugs that not only help people with sleeping problems but also healthy people maximize the quality of their sleep.

“This work opens the door to a new understanding of how to delay and possibly prevent a lot of diseases,” said co-author Ying-Hui Fu. “Our goal really is to help everyone live healthier and longer through getting optimum sleep.”