NIH Research Festival
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OBJECTIVE: Late-life depression (LLD) is associated with increased risk of dementia related to Alzheimer’s disease (AD), yet the mechanism that underlies this relationship remains poorly understood. This study investigated the association of persistent depressive symptoms and LLD with brain amyloid deposition (by florbetapir-PET imaging), a hallmark pathological biomarker of AD.
METHODS: 334 individuals without dementia from the Atherosclerosis Risk in Communities Study had florbetapir-PET scans in late life (ages 67-89). Elevated global and regional brain amyloid deposition was defined as a florbetapir standardized uptake value ratio of >1.2. LLD was assessed cross-sectionally using the 11-item Center for Epidemiological Studies Depression Scale (CES-D) and defined as our primary measure with a score ≥9. Midlife depressive symptoms were assessed at midlife (ages 46-67) using the Maastricht Questionnaire and defined with a score ≥13. Persistent depressive symptoms from mid-to-late life were evaluated by combining these threshold scores. The association between depression measures and amyloid was examined using logistic regression models adjusted for age, race, sex, education level, APOEε4, and vascular risk factors.
RESULTS: Participants (mean age 75.9 years; 57.2% female; 42.5% Black; 26.9% mild cognitive impairment) showed no association between LLD or persistent depressive symptoms and global amyloid deposition. However, LLD was associated with increased amyloid in the amygdala (OR: 4.24, 95% CI: 1.47-13.14).
CONCLUSION: Depression in late life and persistent depressive symptoms are generally not associated with global amyloid deposition. Secondary analyses support an association of LLD with amyloid deposition in the amygdala, a brain region implicated in depression and emotional processing.
Scientific Focus Area: Clinical Research
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