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Sleep and the ageing brain: overview
We spend roughly one third of our lives asleep, but sleep is far from passive downtime. It supports physical restoration, memory consolidation, and clearance of metabolic waste from the brain. New research using high-resolution magnetic resonance imaging (MRI) and machine learning indicates that chronic poor sleep is associated with a brain that appears older than a person’s chronological age — a signal linked in other studies to greater risk of cognitive decline and dementia.
Study design and methods
Population and data sources
Researchers analysed sleep questionnaires and brain MRI data from more than 27,000 UK adults aged 40–70, drawn from a large prospective cohort. This sample size allowed detailed statistical modelling and the exploration of subtle relationships between sleep patterns and brain structure across middle and early older age.
Estimating brain age with imaging and AI
Brain “age” was derived from over 1,000 individual imaging markers extracted from structural MRI scans. These markers included measures such as regional brain volume loss, cortical thinning, and signs of small-vessel damage. A machine learning model was trained on scans from the healthiest participants — those without major illnesses — to learn the typical imaging pattern at each chronological age. The trained model was then applied to the entire cohort to estimate each person’s brain-predicted age. The difference between predicted brain age and actual chronological age (the brain age gap) served as the primary outcome.
Brain aging was estimated from over 1,000 different imaging markers. (LarisaBozhikova/Getty Images/Canva)
How sleep was measured
Sleep is multifaceted, so the study combined five self-reported sleep characteristics into a composite "healthy sleep score":
- Chronotype (morning lark vs evening owl)
- Typical sleep duration (with 7–8 hours considered optimal)
- Symptoms of insomnia
- Habitual snoring
- Excessive daytime sleepiness
Participants were grouped into profiles: "healthy" (four–five healthy traits), "intermediate" (two–three), and "poor" (zero–one). This multidimensional approach captures interactions between traits — for example, someone with insomnia may also report daytime sleepiness, and an evening chronotype often links with shorter sleep duration.
Key findings
The results showed a clear association between poorer sleep profiles and older-looking brains. On average, for every one-point decrement in the healthy sleep score, the brain age gap increased by roughly six months. Individuals with a poor sleep profile had brains that appeared nearly one year older than their chronological age, whereas those with a healthy sleep profile showed little or no gap.
When the five sleep traits were examined separately, two stood out as the strongest contributors to accelerated brain ageing: a late chronotype (habitually staying up late) and abnormal sleep duration (both short and excessively long sleep were linked to worse outcomes). These findings suggest timing and quantity of sleep may be particularly important for long-term brain structure.
Late chronotypes, or late owls, are at risk of faster ageing brains. (M_a_y_a/Getty Images Signature/Canva)
Biological mechanisms: inflammation and waste clearance
Several plausible biological pathways may explain how sleep quality influences brain ageing.
- Inflammation: Blood samples collected at baseline allowed measurement of circulating inflammatory biomarkers. Higher inflammation explained about 10% of the statistical relationship between poor sleep and an older-looking brain, consistent with the hypothesis that sleep disturbance elevates systemic inflammation which, in turn, damages blood vessels and neural tissue.
- Glymphatic clearance: The glymphatic system — a brain-wide network that clears metabolic waste including amyloid and tau proteins — is more active during deep sleep. Disrupted or insufficient sleep could impair this clearance, promoting accumulation of neurotoxic proteins implicated in Alzheimer’s disease.
- Indirect cardiometabolic effects: Chronic poor sleep increases the risk of obesity, type 2 diabetes, hypertension and other cardiovascular conditions, all of which are established risk factors for cerebrovascular damage and accelerated brain ageing.
Clinical and public-health implications
A one-year difference in apparent brain age may seem modest, but even small accelerations in brain ageing can compound over decades and raise the probability of cognitive impairment and dementia. Critically, many aspects of sleep are modifiable. Public-health strategies and clinical interventions that improve sleep behaviours could therefore contribute to preserving brain health across the lifespan.
Practical, evidence-based steps that can help include keeping a consistent sleep schedule, reducing caffeine and alcohol intake in the hours before bedtime, limiting evening screen exposure, and creating a dark, quiet bedroom environment. Where insomnia, obstructive sleep apnoea, or other sleep disorders are suspected, clinical assessment and targeted treatment are warranted.
Study strengths and limitations
Strengths of this research include an unusually large sample size, a multidimensional sleep measurement that goes beyond single-item duration data, and a comprehensive brain-age model built from thousands of MRI features. However, the study relies on self-reported sleep measures rather than objective measures such as actigraphy or polysomnography, and its observational design cannot prove causality. Residual confounding and reverse causation (early brain changes affecting sleep patterns) remain possible explanations that require longitudinal and intervention studies to resolve.
Expert Insight
"This study adds an important piece to the growing evidence that sleep is central to brain health," says Dr. Elena Martinez, a neurologist and sleep researcher. "Machine-learning models provide sensitive tools to detect subtle structural changes. The key takeaway is that improving sleep habits is a realistic strategy to slow brain ageing — and it can be part of routine preventive health care alongside diet and exercise."
Future directions
Future research priorities include using objective sleep monitoring in large cohorts, tracking brain-age trajectories over time, and testing whether sleep-focused interventions (for example treatment of insomnia or sleep apnoea) can reduce the brain age gap and lower subsequent dementia risk. Integrating molecular biomarkers, genetics, and multi-omic data could also clarify mechanisms linking disturbed sleep to neurodegeneration.
Conclusion
This large-scale study links poorer self-reported sleep to a brain that appears older on MRI-based, machine-learning estimates. While inflammation likely explains part of the connection, multiple pathways — including impaired glymphatic clearance and cardiometabolic disease — may contribute. Because sleep is a modifiable behaviour, these findings reinforce the importance of prioritising sleep as a public-health target to preserve cognitive function and healthy brain ageing.
Source: sciencealert
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