"The results highlight the importance of identifying early risk factors when biomarkers are detectable but cognitive impairment is absent," said study author, Arash Salardini, MD, associate professor of cognitive and behavioral neurology at the University of Texas Health, San Antonio, in a press release.
For the study, the researchers analyzed data from 305 cognitively unimpaired participants from the Framingham Heart Study. Participants had an average age of 40 years old, and around half were female. Cortisol was assessed from blood samples and PET imaging was used to assess levels of amyloid and tau 15 years later.
Ultimately, elevated cortisol levels in midlife were linked to higher levels of amyloid deposition later on, especially in postmenopausal women. The researchers noted that postmenopausal hormone changes may accentuate the effects of cortisol on amyloid. No significant associations were observed with tau burden or in men.
While the effect size was modest, the link remained even after controlling for confounding variables such as age. The findings align with well-established findings regarding higher risk and prevalence of AD in women, especially after menopause. The absence of a link with tau build-up also fits within the established timelines of AD pathology, where amyloid build-up typically precedes tau pathology by some years, wrote the researchers in their study.
"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," senior of the study, Sudha Seshadri, founding director of the Biggs Institute, said in a press release.
Longitudinal follow-up is crucial for determining whether the observed changes in amyloid predict clinical onset of Alzheimer's disease, concluded the researchers.
Sources: EurekAlert, Alzheimer's & Dementia
