Scientists agree there’s a connection between poor sleep and dementia, but the causal relationship remains murky – is poor sleep an early sign of the condition or a contributing factor to its development?
A new study published in eBioMedicine – and reported by SciTechDaily – explores how different aspects of sleep relate to the apparent biological age of the brain and why it may age faster than a person’s real age. Led by researchers from the Karolinska Institutet in Sweden, the study utilised data on 27,500 middle-aged and older adults from the UK Biobank, including brain magnetic resonance imaging (MRI), self-reported sleep quality and inflammation levels in the body.
“Our findings provide evidence that poor sleep may contribute to accelerated brain ageing and point to inflammation as one of the underlying mechanisms,” study lead Abigail Dove told SciTechDaily. “Since sleep is modifiable, it may be possible to prevent accelerated brain aging and perhaps even cognitive decline through healthier sleep.”
Researchers used scans and machine learning to assess “brain age,” evaluating more than a thousand MRI-based brain features to determine how the cellular ageing of participants’ brains compared to their chronological age.
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They assessed participants’ sleep quality based on five self-reported factors – chronotype (morning or evening person), sleep duration, insomnia, snoring, and daytime sleepiness – awarding one point per positive measure. Participants were then divided into three groups: healthy (≥4 points), intermediate (2-3 points), or poor (≤1 point) sleep.
“The gap between brain age and chronological age widened by about six months for every 1-point decrease in healthy sleep score,” Dove explained. “People with poor sleep had brains that appeared on average one year older than their actual age.”
Researchers also found that just over 10 percent of the link between poor sleep and older brain age could be attributed to inflammation and other possible mechanisms. Poor sleep could undermine the brain’s waste clearance system, which is active mainly during sleep, or exacerbate known risk factors for brain ageing like cardiovascular disease.
While they emphasise the study’s strengths – large sample size, quality data and the inclusion of several inflammatory biomarkers – they also point out that the UK Biobank study population is “substantially healthier and more socioeconomically advantaged than the general UK population” and that the lengthy study period (nine years) may have ruled out less healthy individuals.
