Cited by 285Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsStress Responses and Cortisol

The DOI matches its Crossref record; 231 of the 231 references it cites were found in a registry or an index; none of the 179 sources its claims cite is checked for support yet.

Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging

Open access

Abstract

Many psychiatric illnesses are associated with early mortality and with an increased risk of developing physical diseases that are more typically seen in the elderly. Moreover, certain psychiatric illnesses may be associated with accelerated cellular aging, evidenced by shortened leukocyte telomere length (LTL), which could underlie this association. Shortened LTL reflects a cell's mitotic history and cumulative exposure to inflammation and oxidation as well as the availability of telomerase, a telomere-lengthening enzyme. Critically short telomeres can cause cells to undergo senescence, apoptosis or genomic instability, and shorter LTL correlates with poorer health and predicts mortality. Emerging data suggest that LTL may be reduced in certain psychiatric illnesses, perhaps in proportion to exposure to the psychiatric illnesses, although conflicting data exist. Telomerase has been less well characterized in psychiatric illnesses, but a role in depression and in antidepressant and neurotrophic effects has been suggested by preclinical and clinical studies. In this article, studies on LTL and telomerase activity in psychiatric illnesses are critically reviewed, potential mediators are discussed, and future directions are suggested. A deeper understanding of cellular aging in psychiatric illnesses could lead to re-conceptualizing them as systemic illnesses with manifestations inside and outside the brain and could identify new treatment targets.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

This review critically examines evidence linking psychiatric disorders to shortened leukocyte telomere length (LTL) and altered telomerase activity as markers of accelerated cellular aging. It concludes that a modest preponderance of evidence supports LTL shortening in MDD, anxiety disorders, and PTSD, but findings are mixed and causality remains undetermined.

Key findings

  • In major depressive disorder (MDD), 11 studies examined LTL; 7 found significantly shorter LTL in currently depressed or mixed mood-disorder groups versus controls, while 4 did not. Effect sizes ranged from 0.04–0.98 (mean Cohen’s d = 0.41; weighted mean Cohen’s d = 0.23).
  • Evidence for bipolar disorder, psychotic disorders, anxiety disorders, and PTSD is mixed; the strongest evidence is for MDD. In bipolar disorder, lithium-treated subjects had significantly increased LTL compared with controls, and in the largest schizophrenia study, LTL was unexpectedly longer in schizophrenia subjects than controls.
  • “Dose-response” evidence is suggestive but mixed: one MDD study found LTL inversely associated with depression severity and 4-year duration; a longitudinal study found internalizing-disorder duration from ages 11–38 predicted LTL at age 38 in men; other studies did not support this pattern.
  • Telomerase activity is less well studied; unmedicated MDD subjects had substantially elevated PBMC basal telomerase activity in a small study, and a meta-analysis of four randomized controlled meditation studies found an effect size of d = 0.46 for increasing PBMC basal telomerase activity.

Methods

  • Design: critical/narrative review, not a formal meta-analysis.
  • Data: MedLine searches through January 2015 for articles containing “telomeres” or “telomerase” plus psychiatric keywords such as depression, bipolar, anxiety, post-traumatic stress, psychosis, or schizophrenia.
  • Analysis: reviewed studies for design, population and control group, diagnostic assessment, sample size and demographics, telomere assay methodology, main findings, effect sizes, and possible confounds; focused primarily on studies using structured DSM diagnoses, with dimensional-symptom studies briefly reviewed in text and not included in summary tables.

Limitations

  • Stated: interpreting LTL is complicated by possible leukocyte-subtype redistribution, uncertain relationship to telomere length in other tissues, differences in DNA extraction and assay methods across laboratories, and even slight DNA degradation yielding spurious measurements.
  • Stated: many subject-level variables and confounds may affect LTL independently of psychiatric illness, including age, sex, genetics, early-life adversity, socioeconomic status, health behaviors, diet, and latent or active viral infections; psychiatric and medical comorbidities and medication effects also complicate attribution.
  • Stated and evident: causality has not been demonstrated, many studies have small sample sizes and methodological differences, and the review is not a formal meta-analysis, so no pooled quantitative estimate or definitive conclusions can be made.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1016/j.neubiorev.2015.05.007

Cites

231 of 231 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

0 of 179 cited sources checked · 0 supported · 0 flagged

Show all 78 claims

  • It may state two separate claims as one. 70
  • Probably not a substantial claim. 19
79 of 79
  • The paper relies on this without support.

    Peripheral markers of cell aging are the only markers that are practical to obtain in living humans.

    “In summary, peripheral markers of cell aging are the only markers that are practical to obtain in living humans.”
  • The paper relies on this without support.

    It is difficult to double-blind behavioral and psychological interventions.

    “However, it is obviously difficult to double-blind such interventions.”
  • The paper relies on this without support.

    Shorter LTL has been linked to current and future medical illnesses and to premature mortality.

    “Evidence of significant LTL shortening in psychiatric illness would be cause for concern, since shorter LTL has been linked to current and future medical illnesses and to premature mortality, although causality has not been demonstrated.”
3 of 3

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 230 references

Cited by

Sorted by citations

Items 101–200 of 285

Metadata

Authors
Lindqvist, D., Epel, E. S., Mellon, S. H., Penninx, B. W., Révész, D., Verhoeven, J. E., Reus, V. I., Lin, J., Mahan, L., Hough, C. M., Rosser, R., Bersani, F. S., Blackburn, E. H., & Wolkowitz, O. M.
Affiliations
  • University of California, San Francisco (US)
  • Amsterdam Public Health (NL)
Corresponding author
Wolkowitz, Owen M.
Venue
Neuroscience & Biobehavioral Reviews
Publisher
Elsevier BV
Published
2015-08
Volume
55
Pages
333-364
ISSN
0149-7634 (ISSN-L)
OpenAlex
W1733523167
Cited by
285
References
230
Citations by year
2026: 6 · 2025: 11 · 2024: 12 · 2023: 23 · 2022: 31 · 2021: 31 · 2020: 24 · 2019: 34 · 2018: 36 · 2017: 33 · 2016: 31 · 2015: 12
FWCI
4.56
Type
journal article
Language
en
Open access
Locations
  • Neuroscience & Biobehavioral Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion)
  • Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
  • VU Research Portal (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
  • IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
  • Lund University Publications (Lund University) (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
Funders
  • National Institute on Aging (R01AG030424, 01AG030424-01A1)
  • National Institute of Mental Health (R01MH083784)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
leukocyte telomere length, cellular aging, mental illness, telomerase activity, depression, inflammation, oxidative stress, cellular senescence, mortality, systemic disease
MeSH terms
Adolescent, Adult, Aged, Mental Disorders, Child, Female, Humans, Leukocytes, Male, Middle Aged, Telomere, Cellular Senescence, Young Adult

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.

A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).

A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review