The study tracked 2,750 cognitively sound adults aged over 50, with the average age being 70, for about five-and-a-half years. Among them, 16 percent reported chronic insomnia, defined as struggling to sleep at least three nights each week for a duration of three months or more.

At the start, participants reported their recent sleep patterns, took annual memory and thinking tests, and some underwent brain scans. 

Researchers examined for white matter hyperintensities—damaged brain tissue areas related to small vessel disease—and amyloid plaques, which are protein deposits associated with Alzheimer’s disease.

At the study’s conclusion, 14 percent of those with chronic insomnia developed mild cognitive impairment or dementia, in contrast to 10 percent of the participants who did not experience insomnia.

Dr. Carvalho further mentioned, “Our findings indicate that insomnia might affect the brain in various ways. This underscores the significance of addressing chronic insomnia—not only to enhance sleep quality but also as a potential measure to safeguard brain health as we grow older.”

Writing in The Conversation Timothy Hearn, Senior Lecturer in Bioinformatics at Anglia Ruskin University, explained the US study’s findings as showing that “insomnia paired with shorter-than-usual sleep was especially harmful.” 

Dr Hearn added: “These poor sleepers already performed as if they were four years older at the first assessment and showed higher levels of both amyloid plaques and white-matter damage. 

“By contrast, insomniacs who said they were sleeping more than usual, perhaps because their sleep problems had eased, had less white-matter damage than average. 

“Why do both amyloid plaques and blood-vessel damage matter? Alzheimer’s disease isn’t driven by amyloid alone. Studies increasingly show that clogged or leaky small blood vessels also speed cognitive decline, and the two disease states can magnify each other. 

“White-matter hyperintensities disrupt the wiring that carries messages between brain regions, while amyloid gums up the neurons themselves. 

“Finding higher levels of both in people with chronic insomnia strengthens the idea that poor sleep may push the brain towards a double hit. 

“These findings add to a growing body of research, from middle-aged civil servants in the UK, to community studies in China and the US, showing that how well we sleep in midlife and beyond tracks closely with how well we think later on. 

“Chronic insomnia appears to accelerate the trajectory towards dementia, not through one pathway but several: by boosting amyloid, eroding white matter and probably raising blood pressure and blood-sugar levels too.”

Dr Hearn added that cognitive behavioural therapy for insomnia, delivered in person or digitally, remains the gold-standard treatment and improves sleep in around 70 percent of patients. 

He went on: “So the relationship is unlikely to be as simple as ‘treat insomnia, avoid dementia’. 

“Poor sleep often co-exists with depression, anxiety, chronic pain and sleep apnoea – all of which themselves hurt the brain. Unravelling which piece of the puzzle to target, and when, will take rigorously designed long-term studies.” 

Professor Jason Ellis—a sleep researcher at Northumbria University in England, who was not involved in the US study—said: “There is evidence that we clear toxins from the brain during sleep, specifically one called beta amyloid, which has also been associated with cognitive decline and neurodegenerative disorders. 

“As such, a lack of consolidated slow wave sleep, over a long period of time, may well increase the risk of cognitive decline. 

“Moreover, Slow Wave Sleep [also known as deep sleep] helps us regulate our endocrine system and immune system and both systems have also been implicated as risk factors for neurodegenerative disorders.”