High midlife stress may raise Alzheimer`s risk in postmenopausal women: Study

High midlife stress may increase the chances of Alzheimer`s disease in women after their menopause, according to a study.

Scientists at the University of Texas Health Science Center at San Antonio, in the US, discovered that high levels of the stress hormone cortisol in midlife can increase amyloid deposition — a hallmark of Alzheimer`s — in postmenopausal women later.

“The results highlight the importance of identifying early risk factors when biomarkers are detectable but cognitive impairment is absent,” said Arash Salardini, Associate Professor at the varsity.

In the study, published in the journal Alzheimer`s & Dementia, the team analysed data from 305 cognitively unimpaired participants in Massachusetts, US.

By comparing midlife cortisol levels at the beginning of a 15-year period with disease indicators at the end, the researchers were able to determine that those levels could serve as an Alzheimer`s disease biomarker.

No significant associations were observed in males or with tau burden, referring to the tau protein that contributes to neuronal dysfunction and death.

“Our work shows that considering sex and hormonal status in understanding Alzheimer`s disease pathogenesis is important and suggests that stress reduction and hormonal interventions may hold promise for Alzheimer`s prevention, especially in at-risk women,” said Sudha Seshadri, from UT Health San Antonio.

Cortisol is a steroid hormone essential for cellular homeostasis, or balance, and the stress response.

In the study, the team hypothesised that cortisol`s impact on Alzheimer`s pathology would be more pronounced in women, especially after menopause, consistent with some previous findings.

Their results showed that postmenopausal women with high midlife cortisol are at increased risk of Alzheimer`s disease. Postmenopausal hormone changes may also amplify cortisol`s effects on amyloid, said the researchers.

Salardini called for further studies to determine whether these early amyloid changes translate into clinical symptoms and to clarify the causal role of cortisol in Alzheimer’s disease development.

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