By Timothy Hearn, Anglia Ruskin University; The Conversation
Participants were classed as having chronic insomnia if their medical records contained at least two insomnia diagnoses a month apart – a definition that captured 16% of the sample. (Pexels Photo)
Staring at the ceiling while the clock blinks 3am doesn’t only sap energy for the next day. A large, long-running US study of older adults has now linked chronic insomnia to changes inside the brain that set the stage for dementia.
The researchers, from the Mayo Clinic in the US, followed 2,750 people aged 50 and over for an average of five and a half years. Every year the volunteers completed detailed memory tests and many also had brain scans that measured two telltale markers of future cognitive trouble: the buildup of amyloid plaques, and tiny spots of damage in the brain’s white matter – known as white-matter hyperintensities.
Participants were classed as having chronic insomnia if their medical records contained at least two insomnia diagnoses a month apart – a definition that captured 16% of the sample.
Compared with people who slept soundly, those with chronic insomnia experienced a faster slide in memory and thinking and were 40% more likely to develop mild cognitive impairment or dementia over the study period.
When the team looked more closely, they saw that insomnia paired with shorter-than-usual sleep was especially harmful. 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.
The study’s models confirmed the well-known effect of carrying the ApoE4 variant; the strongest common genetic risk factor for late-onset Alzheimer’s. Carriers declined more quickly than non-carriers, and the insomnia effect was large enough to be comparable to the effect of having the gene.
Scientists suspect ApoE4 amplifies the damage of sleepless nights by slowing the overnight clearance of amyloid and making blood vessels more vulnerable to inflammation.
Taken together, 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.
That sounds like an obvious next step, but the evidence is mixed. The Mayo Clinic researchers found no clear benefit, or harm, from the sleeping pills its participants were taking. Trials of newer drugs such as orexin blockers have hinted at reductions in Alzheimer-related proteins in spinal fluid, but these studies are tiny and short term.
Cognitive behavioural therapy for insomnia, delivered in person or digitally, remains the gold-standard treatment and improves sleep in around 70% of patients. Whether it also protects the brain is still unproven, although one small trial in people with mild cognitive impairment showed sharper executive function after this type of talk therapy.
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.
Prevention starts early
The participants in Mayo Clinic study were, on average, 70 years old at the start of the study, but other research has shown that routinely sleeping less than six hours a night in your 50s is already linked to higher dementia risk two decades later.
That suggests prevention efforts shouldn’t wait until retirement. Keeping an eye on sleep from midlife, alongside blood pressure, cholesterol and exercise, is a sensible brain-health strategy.
Sleepless nights are more than a nuisance. Chronic insomnia appears to accelerate both amyloid buildup and silent blood-vessel damage, nudging the brain toward cognitive decline – especially in people who already carry the high-risk ApoE4 gene.
Good quality sleep is emerging as one of the modifiable pillars of brain health, but scientists are still working out whether fixing insomnia can truly head off dementia, and at what stage of life interventions will have the greatest payoff.
Timothy Hearn, Senior Lecturer in Bioinformatics, Anglia Ruskin University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
