Your sleep habits may be even more important than you think. A new study from Edith Cowan University (ECU) in Western Australia just found a surprising new link between your nighttime routine and your future risk of Alzheimer’s disease.
The study, which was published in Alzheimer’s & Dementia, a peer-reviewed publication, found that variants of the gene responsible for the brain’s fluid movement interact with a person’s sleep habits, influencing the organ’s structure and cognitive performance long before any signs of Alzheimer’s disease first appear.
The brain’s waste-clearance system, which is most active during sleep, helps flush out the proteins associated with Alzheimer’s. And it doesn’t work the same for everyone. The process’s effectiveness relies on which version of the aquaporin-4 (AQP4) gene a person has, as well as how they sleep.
“Our study shows that individuals carrying certain AQP4 variants showed faster grey matter loss when they reported shorter sleep,” Ayeisha Milligan Armstrong, a postdoctoral research fellow in the Centre for Precision Health, said in a release. “It’s not just which genes you carry—it’s how those genes interact with the world around you. The same variant can look protective or detrimental depending on how someone is sleeping.”
The interaction between sleep and genetics
The study looked at 351 older adults registered in the Australian Imaging, Biomarkers, and Lifestyle study (AIBL). The long-running study collects information from the cohorts every 18 months on biomarkers related to Alzheimer’s disease and lifestyle factors. Since its launch in 2006, AIBL has collected data from 3,045 participants.
The participants in this study were in their mid-70s with no diagnosed cognitive impairments. However, they were showing signs of amyloid buildup, proteins that accumulate abnormally in the brain, causing plaque accumulation known to disrupt cell communication. Their presence is associated with Alzheimer’s disease.
It is important to note that this was not a study of Alzheimer’s patients. Rather, the researchers looked at people who appeared healthy on the surface but were already on a biological trajectory toward the disease.
The scientists tracked 13 common variants of the AQP4 gene against the participants’ self-reported sleep. They then did repeated brain scans and cognitive testing across six different categories including memory, language, and attention.
The results varied depending on which variant of the gene the participant carried. For some participants, shorter sleep tracked with faster loss of gray matter over time. For others, their brain structure changes were mostly associated with how long it took them to fall asleep.
Notably, a longer sleep wasn’t always paired with more brain volume. For at least one variant, people who carried it and logged longer hours actually saw a steeper decline in cognitive ability in comparison with those who slept less.
Cognitive performance followed a similar pattern. Those who experienced sleep disturbances showed different trajectories over time, and the direction of that effect—better or worse—depended on which AQP4 variant they carried.
The findings do not mean a single gene determines anyone’s fate, the researchers caution. But they do suggest that sleep, unlike genetics, is something people can actually change.
“We’ve known for a while that poor sleep and Alzheimer’s risk are linked,” said Tenielle Porter, PhD, another researcher on the study. “What this shows is that rather than assuming everyone at risk follows the same pathway, a more targeted and personalized approach to Alzheimer’s prevention may be needed.”
Is there an ideal amount of sleep to aim for?
Those looking for a clear directive on precisely how much sleep to get to avoid this trajectory may be disappointed. According to professor Simon Laws, the Centre’s director, because the effect of any given sleep pattern depends on which AQP4 variant a person carries, Laws said there’s no single sleep number that applies to everyone.
“The effect shows up as an interaction between a person’s genetic background and their sleep,” he told Inc. “It’s the interaction that matters, not sleep by itself.”
That means well-established sleep advice, like keeping a consistent schedule and treating disorders like sleep apnea, still holds, but Laws said its impact varies depending on a person’s genetics.
He also cautioned against assuming sleep is a bigger or smaller factor than other known risk factors like diet and exercise, since those may also be shaped by individual genetics.
The next step, Laws said, is to run genetically informed clinical trials to see if tailored sleep interventions to a person’s AQP4 can improve long-term brain outcomes.
—Lucia Auerbach
This article originally appeared on Fast Company’s sister website, Inc.com.
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