Chronic Insomnia Linked to Cognitive Decline and Elevated Dementia Risk

Insomnia was linked to cognitive decline and increased risk for cognitive impairment, with reduced sleep associated with worse cognition and brain health, and longer sleep duration protective against white matter damage.

Older adults with chronic insomnia experience a faster rate of cognitive decline and are at higher risk of developing cognitive impairment, according to study results published in Neurology.

Researchers from the Mayo Clinic Study of Aging conducted a population-based cohort study to examine the association between chronic insomnia and longitudinal changes in cognition, amyloid pathology, and cerebrovascular health. All participants underwent annual neuropsychological testing, with imaging assessments providing additional insight into structural and pathological brain changes. Median follow-up was 5.6 years.

A total of 2750 cognitively unimpaired participants were included in a global cognitive mixed-effects model, 2814 were included in a Cox proportional hazards model, 1027 were included in the white matter hyperintensities (WMH) model, and 561 were included in the amyloid-positron emission tomography (PET) analyses. Of those included in the mixed-effects models, the mean (SD) age was 70.3 (9.7), 49.2% were women, and 16.1% were diagnosed with chronic insomnia.

Further studies should investigate the effects of treatment for insomnia and short sleep duration in the trajectory of cognitive decline and neuroimaging biomarkers, including specific classes of hypnotics and CBT-I.

Compared with those without insomnia, individuals with chronic insomnia were older at baseline (72.1 vs 70 years), more often women (58.7% vs 47.3%), and had higher rates of depression, anxiety, cardiometabolic disease, and obstructive sleep apnea.

Chronic insomnia was associated with a faster decline in global cognitive scores (0.011 per year; 95% CI, –0.020 to –0.001; P =.028) and a 40% increased risk of developing cognitive impairment (hazard ratio [HR], 1.4; 95% CI, 1.07-1.85).

Insomnia combined with self-reported reduced sleep duration was linked to poorer baseline cognition (β=–0.211; 95% CI, –0.376 to –0.046; P =.012), higher baseline WMH burden (β=0.147; 95% CI, 0.044-0.249; P =.005), and higher baseline amyloid-PET burden (β=10.5; 95% CI, 0.5-20.6; P =.039). Conversely, participants with insomnia who reported sleeping more than usual demonstrated lower WMH burden (β=–0.142; 95% CI, –0.268 to –0.016; P =.028).

In exploratory analyses, the use of hypnotic medications was not significantly associated with global cognition, risk for cognitive impairment, WMH, or amyloid accumulation. Sensitivity analyses confirmed the findings were consistent, even after accounting for obstructive sleep apnea risk.

Limitations of the study include the lack of objective sleep measures, reliance on diagnostic codes and self-reported sleep duration, incomplete hypnotic medication data, and a predominantly White study population, which may limit generalizability.

“Further studies should investigate the effects of treatment for insomnia and short sleep duration in the trajectory of cognitive decline and neuroimaging biomarkers, including specific classes of hypnotics and CBT-I [cognitive behavioral therapy for insomnia],” the study authors concluded.

Disclosures: This research was supported by the National Institutes of Health, GHR Foundation, and Mayo Foundation for Medical Education and Research, Sleep Number Corporation to Mayo Clinic. Multiple study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures.

References:

Carvalho DZ, Kolla BP, McCarter SJ, et al. Associations of chronic insomnia, longitudinal cognitive outcomes, amyloid-PET, and white matter changes in cognitively normal older adults. Neurology. Published online September 10, 2025. doi:10.1212/WNL.0000000000214155