Categories: Health & Neuroscience

Poor Sleep Health May Accelerate Brain Aging, KI Study Finds

Poor Sleep Health May Accelerate Brain Aging, KI Study Finds

Overview: poor sleep and the aging brain

Bad sleep has long been associated with dementia risk, but it remains unclear whether unhealthy sleep habits drive brain aging or simply reflect early disease symptoms. A large study from Karolinska Institutet addresses this question by examining how sleep patterns relate to brain aging in relation to chronological age. The researchers analyzed 27,500 middle-aged and older individuals from the UK Biobank who underwent brain magnetic resonance imaging (MRI).

Using machine learning, the team estimated each person’s brain age from more than a thousand metrics derived from the MRI data. This allowed them to compare the biological brain age with the actual chronological age, offering a window into how sleep may influence the aging brain beyond what is visible on the calendar.

How brain age was measured

Participants underwent high‑quality MRI scans, and researchers fed thousands of imaging features into predictive models to estimate biological brain age. The aim was to capture subtle structural and microstructural brain changes that accompany aging, enabling a biologically informed assessment rather than relying solely on calendar age.

Sleep quality scoring and groups

Sleep quality was assessed by five self‑reported factors: circadian preference (morning vs evening tendency), average sleep duration, difficulty falling asleep, snoring, and daytime sleepiness. Scores ranged from 0 to a maximum, and participants were categorized into three groups: good sleep (4 points or more), intermediate sleep (2–3 points), and poor sleep (1 point or less).

Across the study population, researchers observed a clear pattern: each one‑point decline in sleep quality was associated with roughly six additional months of brain aging. In practical terms, people with poor sleep appeared, on average, about one year biologically older than their chronological age.

Inflammation as a partial mediator

The study also explored whether systemic inflammation could explain part of the link between poor sleep and older brain age. The results showed that inflammation could account for just over ten percent of the association, suggesting inflammation is one potential driver among several mechanisms connecting sleep health to brain aging.

Possible mechanisms and broader context

Beyond inflammation, several other mechanisms might link poor sleep to accelerated brain aging. One hypothesis involves the brain’s waste clearance system, which cleans away harmful substances during sleep; disturbances to this process could contribute to aging‑related brain changes. Another potential route is the impact of sleep on cardiovascular health, which in turn influences brain function and structure.

Limitations and interpretation

As with many large cohort studies, there are caveats. UK Biobank participants tend to be healthier than the general population, which may affect generalizability. Sleep was assessed through self‑report, which can introduce bias or inaccuracies. The authors also note that observational data cannot establish causality, though the associations point to sleep health as a modifiable factor worth investigating further.

Implications for sleep and cognitive health

The findings offer encouraging implications: because sleep patterns are modifiable, improving sleep quality could potentially slow brain aging and reduce the risk of cognitive decline. Public health strategies that promote regular sleep schedules, adequate duration, and management of sleep disorders might help preserve brain health as we age.

The study in brief

The research was conducted in collaboration with the Swedish School of Sport and Health Sciences and Chinese institutions Tianjin Medical University and Sichuan University, with funding from Alzheimerfonden, Demensfonden, Vetenskapsrådet, and related Swedish foundations. The online publication is in eBioMedicine (October 1, 2025), with the DOI 10.1016/j.ebiom.2025.105941. The researchers report no conflicts of interest.