In a new study, researchers at Karolinska Institute in Sweden report that sleep disturbances in midlife or in late life are linked to a higher risk for dementia in old age.
They found that when people were in their 40s or 50s, insomnia was linked to a 24% increased risk for dementia later in life.
When participants were in their 60s or 70s, terminal insomnia (waking up too early) was linked to a doubled risk for later dementia.
On the other hand, long sleep duration (more than 9 hours of sleep per night) was linked to a fourfold increased risk for later dementia.
The latter finding among this older population may be due to already existing (undiagnosed) dementia-related pathology, as dementia is often linked with sleep disturbances, including increased sleep duration.
The analysis of the study included three population-based studies from Sweden and Finland with large sample sizes of men and women (more than 2 000).
The team has been focusing on lifestyle interventions for dementia. They published the landmark Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (Finger) trial.
The trial showed that a ‘multidomain intervention’ including diet, exercise, cognitive training, and management of vascular risk factors has a positive impact on cognitive functioning.
More recently, many countries are adopting the Finger model to their local settings (e.g. USA, China, Singapore, Canada), within the World-Wide Fingers platform.
The researchers suggest that it is promising that lifestyle changes can positively impact cognition.
So far, there has been little evidence regarding the role of sleep disturbances as a risk factor for dementia.
Their current study indicates that future interventions to prevent dementia may benefit from including interventions to improve sleep.
The team will now continue investigating the association between sleep disturbances and cognitive performance and dementia among different populations, including memory clinic patients.
They will also examine the role of underlying biological mechanisms.
The study is published in Alzheimer’s & Dementia.
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