Abstract
Little is known about the association of cortical Aβ with depression and anxiety among cognitively normal (CN) elderly persons. We conducted a cross-sectional study derived from the population-based Mayo Clinic Study of Aging in Olmsted County, Minnesota; involving CN persons aged ≥ 60 years that underwent PiB-PET scans and completed Beck Depression Inventory-II (BDI-II) and Beck Anxiety Inventory (BAI). Cognitive diagnosis was made by an expert consensus panel. Participants were classified as having abnormal (≥1.4; PiB+) or normal PiB-PET (<1.4; PiB-) using a global cortical to cerebellar ratio. Multi-variable logistic regression analyses were performed to calculate odds ratios (OR) and 95% confidence intervals (95% CI) after adjusting for age and sex. Of 1,038 CN participants (53.1% males), 379 were PiB+. Each one point symptom increase in the BDI (OR = 1.03; 1.00-1.06) and BAI (OR = 1.04; 1.01-1.08) was associated with increased odds of PiB-PET+. The number of participants with BDI > 13 (clinical depression) was greater in the PiB-PET+ than PiB-PET- group but the difference was not significant (OR = 1.42; 0.83-2.43). Similarly, the number of participants with BAI > 10 (clinical anxiety) was greater in the PiB-PET+ than PiB-PET- group but the difference was not significant (OR = 1.77; 0.97-3.22). As expected, depression and anxiety levels were low in this community-dwelling sample, which likely reduced our statistical power. However, we observed an informative albeit weak association between increased BDI and BAI scores and elevated cortical amyloid deposition. This observation needs to be tested in a longitudinal cohort study.
Highlights
Alzheimer’s disease (AD) pathology likely precedes the development of clinical manifestations by several years or decades (Braak and Braak, 1991; Shaw et al, 2007)
Studies have found an association between amyloid deposition with a faster cognitive decline in both cognitively normal elderly (Morris et al, 2009; Chetelat et al, 2012; Knopman et al, 2012; Petersen et al, 2016) and mild cognitive impairment (MCI) subjects (Jack et al, 2010; Jagust et al, 2010)
We sought to examine the association between cortical amyloid deposition, as measured by Pittsburgh compound B positron emission tomography (PiB-PET), depressive and anxiety symptoms in a population-based sample of cognitively normal participants
Summary
Alzheimer’s disease (AD) pathology likely precedes the development of clinical manifestations by several years or decades (Braak and Braak, 1991; Shaw et al, 2007). We and others have reported that depressive (Donovan et al, 2015; Krell-Roesch et al, 2016) and anxiety symptoms (Pink et al, 2017) are associated with neuroimaging biomarkers of AD, FDG-PET and cortical thickness as measured by MRI, among cognitively normal elderly participants. Given the current discussion in the literature on whether prodromal neuropsychiatric symptoms should be assessed on a continuum rather than relying on arbitrary cut-offs (Altman and Royston, 2006; Bjelland et al, 2009; Laborde-Lahoz et al, 2014), we used both continuous and categorical approaches when assessing depressive and anxiety symptoms We hypothesized that both anxiety and depressive symptoms would be associated with higher cortical amyloid deposition as measured by PiB-PET in our sample of community-dwelling cognitively normal elderly persons. Little is known about the association of cortical Aβ with depression and anxiety among cognitively normal (CN) elderly persons
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