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Poor sleep at age 40 was associated with accelerated brain aging patterns at age 55, longitudinal data showed.

A dose-response relationship emerged between the number of poor sleep characteristics early in midlife and brain age 15 years later, reported Clémence Cavaillès, PhD, of the University of California San Francisco, and co-authors in .

People with two or three poor sleep characteristics had a brain age that was 1.6 years older than those with no more than one of six sleep characteristics assessed (β=1.61, 95% CI 0.28-2.93). Those with more than three poor sleep characteristics had a brain age 2.6 years older (β=2.64, 95% CI 0.59-4.69).

Poor sleep characteristics included short sleep duration, bad sleep quality, difficulty initiating sleep, difficulty maintaining sleep, early morning awakening, and daytime sleepiness.

Sleep disturbances have been linked with poor cognitive performance and an increased risk of dementia, including Alzheimer's disease, Cavaillès noted.

"However, most studies involve older adults, which raises concerns given the long neurodegenerative process in conditions like Alzheimer's disease, where the lesions -- beta-amyloid plaques and tau tangles -- accumulate years before symptoms appear," she told MedPage Today.

"Advanced brain aging is associated with cognitive decline and Alzheimer's-related atrophy patterns," Cavaillès continued. "Therefore, poor sleep may be an important target for early interventions aimed at preventing neurocognitive decline, even before amyloid and tau accumulation begins."

Good quality sleep is very important, observed Nicolas Cherbuin, PhD, of the Australian National University in Canberra, who wasn't involved with the study.

"That's because one of sleep's functions is to help remove toxic substances, malformed protein, and damaged cell debris from the brain," which is increasingly important with age, he told MedPage Today.

Other research has linked poor sleep quality in midlife with or cognitive problems, Cherbuin pointed out.

"Midlife is when accumulating damage becomes more easily detectable and it is also a period in life where risk factors for brain and cognitive aging -- such as poor mental health, stress, obesity, diabetes, hypertension, hypercholesterolemia, and sedentary lifestyle -- combine and become increasing concerns," he said. "Consequently, good sleep quality at midlife and thereafter becomes even more important for brain health, thinking skills, and mental well-being."

Cavaillès and colleagues used , a long-term study of cardiovascular disease risk in young adults, to analyze baseline sleep data in 589 participants.

Sleep characteristics were self-reported. Brain MRIs were obtained 15 years later and were used to determine brain age based on atrophy using a machine-learning approach.

Mean baseline age was 40.4 (±3.4) years. About half (53%) of participants were women, and 39% were Black.

Around 70% of participants reported no more than one poor sleep characteristic; 22.4% reported two or three, and 8.3% reported more than three. Compared with participants who had one or no poor sleep characteristics, those with two or more were more likely to be Black, have hypertension or depressive symptoms, and be less educated.

After a mean follow-up duration of 15 years, the mean brain age was 54.3, and the mean chronological age was 55.3 years.

A subsample of 566 participants reported sleep information 5 years after baseline. These data showed that persistent bad sleep quality, difficulty initiating and maintaining sleep, early morning awakening, and daytime sleepiness each were associated with older brain age at the 15-year follow-up.

The findings in this study "are critical because they demonstrate that the link between sleep disturbances and brain health extends beyond older adulthood, suggesting that poor sleep in early midlife may already contribute to accelerated brain aging," Cavaillès said.

The study had limitations, the researchers acknowledged. Sleep characteristics were self-reported and may have been misclassified. Brain age may have been influenced by unmeasured neuropathology. Because this was an observational study, a causal relationship can't be assumed.

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