Chronic insomnia is associated with accelerated development of dementia
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Sleepless nights aren't just about being tired the next day.
A large long-term study of elderly people in the United States has shown that chronic insomnia is associated with changes in the brain that set the stage for dementia. This is reported by the publication The Conversation.
Scientists from the Mayo Clinic (Mayo Clinic) observed 2,750 people aged 50 years and older on average for five and a half years. Once a year, the participants underwent detailed memory and thinking tests, and some volunteers had regular MRI scans and other brain tests. Experts were interested in two key markers of future cognitive problems: the accumulation of amyloid plaques and small foci of damage to the brain's white matter - so-called white matter hyperintensities.
Chronic insomnia was defined as when a person's medical records showed at least two diagnoses of insomnia at least one month apart. By this criterion, about 16% of participants fell into the chronic insomnia group.
Compared to people without pronounced sleep problems, those with chronic insomnia had a faster decline in memory and other cognitive functions. They were about 40% more likely to develop mild cognitive impairment or dementia during the follow-up period.
When the researchers looked at the data in more detail, it turned out that a particularly vulnerable group were those who had insomnia combined with shortened sleep. These participants already performed as if they were an average of four years older on the first test, and their brains showed higher levels of amyloid plaques and white matter damage.
In contrast, people with insomnia who reported sleeping longer than usual (possibly on a background of better sleep or treatment) had lower average levels of white matter damage than the others.
According to the authors, it is important that such patients have a "double blow" at once: amyloid deposits disrupt the work of neurons, and white matter hyperintensities impair the conduction of signals between brain regions due to damage to small vessels. Current research shows that it's not just amyloid that causes Alzheimer's disease: small vessel conditions also significantly accelerate cognitive decline, and the combination of these problems amplifies the overall damage.
The study models also confirmed the known role of the ApoE4 gene variant, the strongest common genetic risk factor for late-onset Alzheimer's disease. ApoE4 carriers declined in cognitive performance faster than others, and the effect of chronic insomnia was comparable in magnitude to the impact of this gene. The scientists suggest that ApoE4 may exacerbate the harms of sleep deprivation by slowing the nocturnal "removal" of amyloid from the brain and making blood vessels more vulnerable to inflammation.
The findings add to those of other large studies, from a cohort of British civil servants to general population samples in China and the US: sleep quality in middle age and old age is closely linked to the state of cognitive function later in life. Chronic insomnia likely accelerates the trajectory to dementia through several pathways at once - via amyloid, white matter damage, and elevated blood pressure and blood sugar levels.
That said, the issue of treating insomnia remains an open question. Mayo Clinic experts found no clear benefit or harm from the sleeping pills that participants took. Initial small studies of new drugs, such as orexin blockers, have shown a possible reduction in the levels of Alzheimer's-related proteins in the cerebrospinal fluid, but these studies are still too small and short-term.
Cognitive-behavioural therapy for insomnia - face-to-face or digitally - is considered the gold standard. It improves sleep in about 70% of patients. However, there is no conclusive evidence that such therapy actually protects the brain from dementia, although a small study in people with mild cognitive impairment showed improvement in executive function after a course of such therapy.
The authors emphasise that the link is unlikely to be reduced to the simple principle of "cure insomnia - avoid dementia". Poor sleep is often combined with depression, anxiety, chronic pain, sleep apnoea - and all of these conditions themselves are harmful to the brain. It takes long, carefully designed studies to figure out which "piece of the puzzle" to target and when.
Nevertheless, prevention should start early. Although in the Mayo Clinic study the average age of participants at the start was around 70, other work has shown: regular sleep of less than six hours at age 50 is already associated with an increased risk of dementia 20 years later. This means that it's worth monitoring your sleep before you retire - along with controlling your blood pressure, cholesterol and physical activity.
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Elena Rasenko writes about science, healthy living and psychology news, and shares her work-life balance tips and tricks.










