Cited by 20Telomeres, Telomerase, and SenescenceStress Responses and CortisolTreatment of Major Depression

Longueur des télomères dans le cortex des patients atteints de troubles dépressifs

Teyssier, J.-R., Ragot, S., Donzel, A., Chauvet-Gelinier, J.-C.·2010·L Encéphale

Abstract

Background Telomeres are complex structures formed by the end of the DNA molecule at the tip of chromosomal arms. The telomeric sequence, which results from the repetition of the hexanucleotide TTAGGG, is partly single strand and is associated with more than ten proteins, including the enzyme telomerase. Because of the characteristics of the DNA replication process, only telomerase is able to elongate the telomeric sequence. Since the telomerase gene is repressed in virtually all the somatic cells, telomeres progressively shorten at each S phase of the cell cycle, and this shortening is accelerated by oxidative stress. A critically shortened telomere activates the genetic program of cell senescence and/or apoptosis. The telomere length measured in peripheral blood leucocytes is considered a reliable marker of biological age, mortality risk and exposure to various pathological conditions, including cardiovascular disease, dementia and metabolic syndrome. Telomere erosion has been observed in psychiatric disorders including schizophrenia and mood disorders, suggesting an accelerated aging of 10 to 20 years. Whether this peripheral dynamic is reflected by a similar pattern in the brain remains unknown. To address this issue, we have measured the telomere length in the occipital DNA cortex of 24 patients with major depressive disorder and 12 controls (donated by the Stanley Research Institute).Methodology The mean telomere length has been evaluated by a real time quantitative PCR technique, which amplified the telomere sequence and a reference single copy sequence. Results have been expressed by the ratios of Ct obtained for the two amplification curves.Results The mean Ct values were strictly identical (0.79 ± 0.001) and the 36 PCR curves were coincident.Discussion This study demonstrates for the first time that there is no shortening of telomeres in the cortex of patients with depressive disorder. Previous results have shown that in normal tissues telomeres length is inversely correlated to age, even in non proliferating tissues, but that the change is minimal in the brain. Thus, although consistent evidence for the role of a systemic and brain inflammation associated oxidative stress in depression has been provided, it must be concluded that the cerebral state of telomeres is not affected by the mechanism operating in the leucocytes. This observation raises the issue of the relation between the psychiatric pathological process and the peripheral telomere marker. It suggests the existence of specific telomere stabilizing factors in the cortex cells.

Integrity signals

Registry

Crossref · 10.1016/j.encep.2010.04.004

Cites

18 of 18 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • Two post-mortem studies of TL in cerebellar gray matter and occipital cortex found no significant differences between MDD subjects and controls, although correlations with LTL were not assessed.

    “Two post-mortem studies of TL in cerebellar gray matter and occipital cortex found no significant differences between MDD subjects and controls, although correlations with LTL were not assessed (Teyssier et al., 2010; Zhang et al., 2010).”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Teyssier, J.-R., Ragot, S., Donzel, A., & Chauvet-Gelinier, J.-C.
Affiliations
CHU Dijon Bourgogne (FR)
Corresponding author
Teyssier, J.-R.
Venue
L Encéphale
Publisher
Elsevier BV
Published
2010-12
Volume
36
Issue
6
Pages
491-494
ISSN
0013-7006 (ISSN-L)
OpenAlex
W1982079760
Cited by
20
References
18
Citations by year
2025: 1 · 2022: 1 · 2019: 5 · 2018: 1 · 2016: 4 · 2015: 3 · 2014: 1 · 2013: 1 · 2012: 2
FWCI
0.87
Type
journal article
Language
fr
Open access
closed
Locations
  • L Encéphale (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Keywords
telomere length, depression, occipital cortex, telomere shortening, oxidative stress, inflammation, premature aging, telomerase, biological age, mood disorders, schizophrenia, psychosocial stress, brain aging biomarkers
MeSH terms
Adult, Affective Disorders, Psychotic, Age Factors, Cause of Death, Major Depressive Disorder, Female, France, Humans, Leukocytes, Male, Middle Aged, Occipital Lobe, Reference Values, Suicide, Polymerase Chain Reaction, Telomere, Apoptosis

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.

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