A study from Sweden indicates that insomnia may weaken biological defenses against Alzheimer’s disease, with stress exacerbating this effect. Researchers at Karolinska Institutet, published in the Journal of Neurology, linked a history of stressful events to greater amyloid accumulation in the brain, particularly among individuals experiencing moderate to severe insomnia. In contrast, participants who reported healthy sleep patterns did not show this correlation.
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The research was part of the Cortisol and Stress in Alzheimer’s disease cohort (Co-STAR), involving 124 patients from the Karolinska University Hospital memory clinic between 2014 and 2017. None had dementia at the time of the study; 56 were diagnosed with subjective cognitive impairment, and 68 with mild cognitive impairment. The average age of participants was 61.5 years, with nearly 60 percent being women.
Researchers utilized cerebrospinal fluid collected through lumbar punctures during routine assessments to measure Alzheimer’s biomarkers—beta-amyloid 42, total tau, and phosphorylated tau at position 181. Stress was evaluated using the Perceived Stress Scale and a life events inventory that included an array of stressful experiences, while insomnia symptoms were assessed using the Karolinska Sleep Questionnaire.
The study revealed a complex interaction between insomnia and stress, particularly affecting cerebrospinal fluid amyloid levels. In participants with low insomnia symptoms, higher exposure to stress correlated with increased amyloid 42 levels. Conversely, those with moderate to high insomnia exhibited lower levels of amyloid 42 in relation to stress exposure. This pattern held for both chronic and acute stressors but leveled off at the highest insomnia scores.
Interestingly, the interaction was significant only for amyloid, with no notable relationship found with total tau or phosphorylated tau, aligning with previous studies that connect sleep disturbances primarily to amyloid accumulation.
The researchers suggest that chronic stress may disrupt hormone regulation, altering the production pathways for amyloid proteins. Additionally, the glymphatic system, which cleanses the brain waste, operates primarily during sleep. Insomnia could impair this clearance, resulting in higher amyloid levels from increased production and reduced disposal.
The study also explored sex differences, noting that while the direction of the interactions was consistent across genders, the relationship between stress exposure and amyloid levels differed. Higher amyloid levels correlated with greater stress in men, while women showed the opposite trend.
Despite these findings, limitations exist, including the cross-sectional design, self-reported data, and a small sample size that restricts definitive claims about sex differences. Future longitudinal studies are necessary to further investigate these relationships, ideally including object measures for stress and sleep patterns.
The implications could be significant for dementia prevention strategies, emphasizing the importance of managing insomnia, especially among those experiencing high levels of stress, as part of a multifaceted approach.