Are apathy and depression independently associated with longitudinal trajectories of cortical atrophy in mild cognitive impairment?
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Objectives To examine whether depression and apathy are independently associated with longitudinal trajectories of cortical atrophy in the entorhinal cortex compared with frontal subregions previously implicated in late-life mood disturbance.Methods Data from 334 participants classified as having mild cognitive impairment in the Alzheimer's Disease Neuroimaging Initiative (ADNI) were analyzed by using multilevel models for change adjusted for age, global cognitive status, and total intracranial volume at enrollment. Participants in ADNI were recruited from >50 clinical research sites in the United States and Canada. Depression and apathy were identified by informants using the Neuropsychiatric Inventory Questionnaire. Serial magnetic resonance imaging was performed on 1.5-Tesla scanners according to the standardized ADNI-1 protocol on an average of 5 occasions over an average of 30.5 months. Regional cortical thickness values were derived from longitudinal data processing in FreeSurfer version 4.4.Results Depression was associated with reduced cortical thickness in the entorhinal cortex at baseline and accelerated atrophy in the anterior cingulate cortex. Similar relationships between depression and the orbitofrontal cortex and between apathy and the anterior cingulate cortex were not significant.Conclusions In mild cognitive impairment, depression signs are a better marker of longitudinal cortical atrophy than apathy. Results are consistent with hypotheses that depression is an early sign of a more aggressive neurodegenerative process or that depression lowers brain reserve capacity, allowing for more rapid progression of Alzheimer disease neuropathology.
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Depression in Alzheimer's disease is associated with reduced entorhinal cortical thickness at baseline and with accelerated atrophy in anterior cingulate cortex.
“They found Depression to be associated with reduced entorhinal cortical thickness at baseline and with accelerated atrophy in ACC.”
From Neuropsychiatric symptoms in Alzheimer's disease: what might be associated brain circuits? (2015) · cites this paper as Zahodne et al., 2013
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Neurologic Changes and Depression
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- Authors
- Zahodne, L. B., Gongvatana, A., Cohen, R. A., Ott, B. R., & Tremont, G.
- Affiliations
- Columbia University (US)
- Brown University (US)
- Venue
- The American Journal of Geriatric Psychiatry
- Publisher
- Elsevier BV
- Published
- 2013-11
- Volume
- 21
- Issue
- 11
- Pages
- 1098-1106
- ISSN
- 1064-7481 (ISSN-L)
- PMC
- PMC3797189
- OpenAlex
- W2029025179
- Cited by
- 72
- References
- 43
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 6 · 2023: 3 · 2022: 11 · 2021: 9 · 2020: 4 · 2019: 5 · 2018: 2 · 2017: 3 · 2016: 6 · 2015: 10 · 2014: 3 · 2013: 2
- FWCI
- 4.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Geriatric Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Alzheimer's Association (U01 AG024904)
- Bristol-Myers Squibb (U01 AG024904, AG024904)
- Eli Lilly and Company (U01 AG024904, AG024904)
- Pfizer (AG024904, U01 AG024904)
- AstraZeneca
- Biogen (U01 AG024904, AG024904)
- F. Hoffmann-La Roche (AG024904, U01 AG024904)
- Medpace (U01 AG024904)
- Meso Scale Diagnostics (U01 AG024904, AG024904)
- Synarc (U01 AG024904)
- Alzheimer's Disease Neuroimaging Initiative (U01AG024904, AG024904)
- Amorfix Life Sciences
- BioClinica (U01 AG024904, AG024904)
- Novartis Pharmaceuticals Corporation (U01 AG024904, AG024904)
- Northern California Institute for Research and Education (U01 AG024904)
- Bayer HealthCare
- Eisai (U01 AG024904, AG024904)
- Servier (AG024904, U01 AG024904)
- IXICO (AG024904, U01 AG024904)
- National Institutes of Health (3u01ag024904-10s2, U01-AG024904, AG024904)
- Genentech (AG024904, U01 AG024904)
- University of California, Los Angeles
- University of California, San Diego
- Canadian Institutes of Health Research (U01 AG024904)
- National Institute on Aging (U01-AG-024904, U19AG010483, P30AG028740)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cancer-related cognitive impairment studies
- Keywords
- depression, apathy, mild cognitive impairment, cortical atrophy, entorhinal cortex, anterior cingulate cortex, orbitofrontal cortex, cortical thickness, longitudinal brain changes, Alzheimer's disease, brain reserve, mood disturbance
- MeSH terms
- Aged, Aged, 80 and over, Aging, Atrophy, Cerebral Cortex, Depression, Female, Humans, Male, Middle Aged, Models, Psychological, Neuropsychological Tests, Disease Progression, Apathy, Neuroimaging, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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