Depression and hippocampal volume in the aging brain: an epidemiological investigation
Bibliographic record
Abstract
Background: Magnetic resonance imaging (MRI) studies have reported that patients with depression have smaller hippocampal volume (HcV) than healthy controls. However, the temporality of this association is unresolved. Two main hypotheses are proposed to explain the depression-HcV relationship. The neurotoxicity hypothesis suggests that HcV atrophy results from biological and neurochemical alterations that accompany depression and stress; an alternative hypothesis is that reduced HcV could be a susceptibility factor for depression. Disentangling the temporality of the depression-HcV atrophy relationship is of particular interest in older adults as it can help unravel the complex processes underlying aging-related cerebral, cognitive, and mood changes. Research objectives: The overall aim of this thesis was to examine the two main hypotheses on the temporal relationship between depression and HcV atrophy in a population-based sample of older adults; the specific objectives were: 1) To assess whether history of previous depression and more proximal depressive symptoms are related to HcV atrophy; 2) To estimate the association between life-course socioeconomic position (SEP), as a proxy for increased stress, and HcV atrophy; 3) To examine whether HcV atrophy is associated with subsequent depressive symptoms. Study population: Data come from the Three-City-Dijon-MRI cohort, a prospective population-based French cohort of older adults (n=1328, age=65-80 years) who were followed biennially for over ten years and who had two cerebral MRI scans, at baseline and four-year follow-up. Manuscript 1- Examining the neurotoxicity hypothesis: We estimated the association between history of previous depression and proximal depressive symptoms (Center for Epidemiologic Studies-Depression (CES-D) scale) and both baseline HcV and rate of HcV atrophy. We found that baseline depressive symptoms were associated with smaller HcV in women; in contrast, history of depression and more proximal depressive symptoms were associated with faster HcV atrophy in women but not in men. Our findings also showed that treatment for depression was associated with slower HcV atrophy in men and women. Manuscript 2- Life-course SEP and HcV atrophy: To further explore the neurotoxicity hypothesis and its implication that stressful conditions may contribute to HcV atrophy, we examined the relationships of SEP with HcV and HcV atrophy using three life-course SEP models: (i) the sensitive/critical-period model which focused on SEP at three periods over the life-course: childhood SEP (parental education), early-adulthood SEP (participants’ education), and mid-life SEP (participants’ socioprofessional attainment); (ii) life-course cumulative SEP; and (iii) social-mobility of life-course SEP trajectories. Childhood and early-adulthood SEP were not related to HcV outcomes. Participants with lower socioprofessional attainment in mid-life had smaller HcV and faster HcV atrophy. Results also suggested that cumulative low SEP and disadvantageous SEP trajectories over the life-course were associated with faster HcV atrophy. Manuscript 3- Exploring the hypothesis that HcV atrophy is a susceptibility factor for depression: We used linear mixed-models to estimate the associations between rate of HcV atrophy and (i) average-over-follow-up depressive symptoms (CES-D scores) measured biennially over the subsequent six years and (ii) change in depressive symptoms. Results indicated that, in women, faster HcV atrophy was associated with more average over-follow-up depressive symptoms and with worsening of symptoms over the two subsequent years. No association was detected in men. Conclusion: Our findings suggest a complex and bi-directional relationship between HcV atrophy and depressive symptoms in women but not in men. The results also highlight the role for stress-related experiences (previous depression and lower SEP) in explaining some of the variability in HcV atrophy at older age.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.002 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.002 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".