A 2026 study of Swedish memory-clinic patients without dementia found a relationship between stressful life events, insomnia symptoms and a cerebrospinal-fluid marker associated with amyloid in the brain.
The pattern was seen mainly among people with moderate-to-high insomnia symptoms. It does not show that stress or insomnia causes Alzheimer’s-related brain changes, nor that treating either one lowers amyloid or dementia risk.
What the researchers measured
The analysis used baseline data from the Co-STAR study at the Karolinska University Hospital memory clinic in Stockholm. Participants were first-time patients recruited between 2014 and 2017.
After exclusions, 124 people remained. Their average age was 61.5 years, and 60% were women. Fifty-six had subjective cognitive impairment and 68 had mild cognitive impairment. Routine lumbar punctures provided cerebrospinal-fluid samples for 103 participants.
The researchers assessed stressful life events, insomnia symptoms and three cerebrospinal-fluid markers: amyloid-beta 42 (Aβ42), total tau and phosphorylated tau. The models accounted for age, sex, education, sleep-medication use and depressive symptoms.
The main finding was an interaction
More lifetime stressful events were linked with lower Aβ42 only when insomnia symptoms were moderate to high. In cerebrospinal fluid, lower Aβ42 is considered a sign associated with more amyloid in the brain.
The statistical finding came from the difference between the stress-related patterns at different insomnia levels. The individual estimates at lower and higher insomnia levels were not statistically significant on their own, but the overall interaction was significant.
Recent events occurring within the previous five years showed a similar pattern. Among people with more insomnia symptoms, each additional recent event was associated with Aβ42 about 0.31 standard deviations lower. Among those with fewer insomnia symptoms, the estimate was close to zero.
Chronic events, including experiences such as a close relative’s serious illness, also showed a stress-insomnia pattern. However, the direction of the association differed across insomnia levels in that analysis.
When the researchers modeled insomnia as a curved rather than a straight-line relationship, lower insomnia was associated with higher Aβ42 as events increased, average-to-high insomnia with lower Aβ42, and very high insomnia with the association disappearing.
Other markers did not show the same result
Stress and insomnia did not interact in relation to total tau or phosphorylated tau. The researchers noted that the sample may have been too small to detect a weaker interaction involving tau.
Insomnia symptoms by themselves were associated with higher cerebrospinal-fluid Aβ42 in this sample. That result underscores why the study cannot be reduced to a simple claim that more insomnia equals more amyloid.
People reporting more stress during the previous month also reported more insomnia symptoms. An apparent interaction between recent perceived stress and insomnia disappeared after the researchers included the curved insomnia pattern.
Why the findings are limited
This was a cross-sectional study, meaning stress, sleep and cerebrospinal-fluid markers were measured at about the same time. It cannot establish whether stressful events and insomnia came before amyloid-related changes, whether biological changes contributed to sleep and stress problems, or whether another factor influenced both.
Insomnia was assessed with three questionnaire items rather than a clinical diagnosis or sleep tracking. Life events were recalled over long periods, which can also affect measurement.
The analysis was small and involved memory-clinic patients in Sweden, so the findings may not apply to the general older population. It measured biomarkers but did not include amyloid PET scans, later cognitive outcomes or follow-up for dementia. The researchers also tested several stress measures against multiple markers, an approach that makes cautious interpretation important.
What people can take from the study
The results support further research into how persistent sleep problems and stressful experiences may relate to Alzheimer’s-related biology. Possible pathways discussed by the researchers included increased amyloid production, reduced clearance during insomnia and inflammation, but this study did not test those mechanisms.
The findings do not show that reducing stress or treating insomnia prevents Alzheimer’s disease. For persistent sleep trouble, the source describes cognitive behavioral therapy for insomnia, or CBT-I, as the usual first-line treatment. The study itself does not establish whether CBT-I or any other intervention changes cerebrospinal-fluid amyloid.
AI tools were used to assist with the preparation of this article.
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