Journal
AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
Volume 25, Issue 7, Pages 683-693Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jagp.2016.12.017
Keywords
18F-fluorodeoxyglucose positron emission tomography; alzheimer disease; apathy; mild cognitive impairment; metabolism
Categories
Funding
- Massachusetts Alzheimer's Disease Research Center Neurodiscovery Grant
- Harvard Medical School Department of Psychiatry Dupont Warren Fellowship
- Rogers Family Foundation
- Muriel Silberstein Alzheimer's Disease Research Fund
- Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health) [U01 AG024904]
- DOD ADNI (Department of Defense) [W81XWH-12-2-0012]
- Eisai, Inc.
- Eli Lilly and Company
- Avid Radiopharmaceuticals
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Objectives: Apathy is among the earliest and most pervasive neuropsychiatric symptoms in prodromal and mild Alzheimer disease (AD) dementia that correlates with functional impairment and disease progression. We investigated the association of apathy with regional 18F-fluorodeoxyglucose (FDG) metabolism in cognitively normal, mild cognitive impairment, and AD dementia subjects from the Alzheimer's Disease Neuroimaging Initiative database. Design: Cross-sectional and longitudinal studies. Setting: 57 North American research sites. Participants: 402 community dwelling elders. Measurements: Apathy was assessed using the Neuropsychiatric Inventory Questionnaire. Baseline FDG metabolism in five regions implicated in the neurobiology of apathy and AD was investigated in relationship to apathy at baseline (cross-sectional general linear model) and longitudinally (mixed random/fixed effect model). Covariates included age, sex, diagnosis, apolipoprotein E genotype, premorbid intelligence, cognition, and antidepressant use. Results: Cross-sectional analysis revealed that posterior cingulate hypometabolism, diagnosis, male sex, and antidepressant use were associated with higher apathy scores. Longitudinal analysis revealed that the interaction of supramarginal hypometabolism and time, posterior cingulate hypometabolism, and antidepressant use were associated with higher apathy scores across time; only supramarginal hypometabolism was positively related to rate of increase of apathy. Conclusions: Results support an association of apathy with hypometabolism in parietal regions commonly affected in early stages of AD, rather than medial frontal regions implicated in the neurobiology of apathy in later stages. Further work is needed to substantiate whether this localization is specific to apathy rather than to disease stage, and to investigate the potential role of AD proteinopathies in the pathogenesis of apathy.
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