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Of sound mind and body: depression, disease, and accelerated aging
Wolkowitz OM, Reus VI, Mellon SH.. Dialogues in clinical neuroscience, 2011-01-01
Topic: Risk, prevention and care in population studies
Major depressive disorder (MDD) is associated with a high rate of developing serious medical comorbidities such as cardiovascular disease, stroke, dementia, osteoporosis, diabetes, and the metabolic syndrome. These are conditions that typically occur late in life, and it has been suggested that MDD may be associated with "accelerated aging." We review several moderators and mediators that may accompany MDD and that may give rise to these comorbid medical conditions. We first review the moderating effects of psychological styles of coping, genetic predisposition, and epigenetic modifications (eg, secondary to childhood adversity). We then focus on several interlinked mediators occurring in MDD (or at least in subtypes of MDD) that may contribute to the medical comorbidity burden and to accelerated aging: limbic-hypothalamic-pituitary-adrenal axis alterations, diminution in glucocorticoid receptor function, altered glucose tolerance and insulin sensitivity, excitotoxicity, increases in intracellular calcium, oxidative stress, a proinflammatory milieu, lowered levels of "counter-regulatory" neurosteroids (such as allopregnanolone and dehydroepiandrosterone), diminished neurotrophic activity, and accelerated cell aging, manifest as alterations in telomerase activity and as shortening of telomeres, which can lead to apoptosis and cell death. In this model, MDD is characterized by a surfeit of potentially destructive mediators and an insufficiency of protective or restorative ones. These factors interact in increasing the likelihood of physical disease and of accelerated aging at the cellular level. We conclude with suggestions for novel mechanism-based therapeutics based on these mediators.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Wolkowitz, O. M., Reus, V. I., & Mellon, S. H. (2011). Of sound mind and body: depression, disease, and accelerated aging. Dialogues in clinical neuroscience. https://doi.org/10.31887/dcns.2011.13.1/owolkowitz
Vancouver
Wolkowitz OM, Reus VI, Mellon SH. Of sound mind and body: depression, disease, and accelerated aging. Dialogues in clinical neuroscience. 2011. doi:10.31887/dcns.2011.13.1/owolkowitz. PMID: 21485744.
BibTeX
@article{wolkowitz2011-21485744,
author = {Wolkowitz, O. M. and Reus, V. I. and Mellon, S. H.},
title = {{Of sound mind and body: depression, disease, and accelerated aging}},
journal = {Dialogues in clinical neuroscience},
year = {2011},
doi = {10.31887/dcns.2011.13.1/owolkowitz},
pmid = {21485744},
url = {https://doi.org/10.31887/dcns.2011.13.1/owolkowitz}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Major depressive disorder (MDD) is associated with a high rate of developing serious medical comorbidities such as cardiovascular disease, stroke, dementia, osteoporosis, diabetes, and the metabolic syndrome.
- These are conditions that typically occur late in life, and it has been suggested that MDD may be associated with "accelerated aging." We review several moderators and mediators that may accompany MDD and that may give rise to these comorbid medical conditions.
- We conclude with suggestions for novel mechanism-based therapeutics based on these mediators.
Why it matters
This review discusses how major depressive disorder is associated with a higher rate of developing conditions including dementia, and proposes that depression may be linked to accelerated aging through several biological processes. It is a review of proposed mechanisms and does not test a treatment or prevention for Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Dialogues in clinical neuroscience) |
| Journal's citation record | 2 / 4 | Dialogues in Clinical Neuroscience: journal h-index 154 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2011 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 216 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 12.7 citations a year over 17 year(s) since 2011 |
| Impact for its field and year | 3 / 6 | Cited 7.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 2 / 4 | Cited 29 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Synthia H. Mellon: h-index 63 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, San Francisco: institution h-index 1,915 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 21485744) |
| Free to read | 2 / 2 | Free to read |
| Total | 44 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.31887/dcns.2011.13.1/owolkowitz
- PubMed: 21485744
- Original source →
- Free full text: Dialogues in Clinical Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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