Longueur des télomères dans le cortex des patients atteints de troubles dépressifs
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
Cites
Statistics
Claims the paper makes
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).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Teyssier et al., 2010
Cites
Telomere measurement by quantitative PCR
Cawthon, R. (2002) · Nucleic Acids Research · doi:10.1093/nar/30.10.e47 · Cited by 3,492 · see citing works
Accelerated telomere shortening in response to life stress
Epel, E. S., Blackburn, E. H., Lin, J., Dhabhar, F. S., Adler, N. E., Morrow, J. D., & Cawthon, R. M. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0407162101 · Cited by 3,002 · see citing works
Oxidative stress shortens telomeres
von Zglinicki, T. (2002) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(02)02110-2 · Cited by 2,524 · see citing works
Association between telomere length in blood and mortality in people aged 60 years or older
Cawthon, R. M., Smith, K. R., O'Brien, E., Sivatchenko, A., & Kerber, R. A. (2003) · The Lancet · doi:10.1016/s0140-6736(03)12384-7 · Cited by 1,761 · see citing works
Telomeres and human disease: ageing, cancer and beyond
Blasco, M. A. (2005) · Nature Reviews Genetics · doi:10.1038/nrg1656 · Cited by 1,690 · see citing works
Aubert, G., & Lansdorp, P. M. (2008) · Physiological Reviews · doi:10.1152/physrev.00026.2007 · Cited by 1,188 · see citing works
Oxidative stress in psychiatric disorders: evidence base and therapeutic implications
Ng, F., Berk, M., Dean, O., & Bush, A. I. (2008) · The International Journal of Neuropsychopharmacology · doi:10.1017/s1461145707008401 · Cited by 1,069 · see citing works
Simon, N. M., Smoller, J. W., McNamara, K. L., Maser, R. S., Zalta, A. K., Pollack, M. H., Nierenberg, A. A., Fava, M., & Wong, K.-K. (2006) · Biological Psychiatry · doi:10.1016/j.biopsych.2006.02.004 · Cited by 516 · see citing works
Telomere lengths are characteristic in each human individual
Takubo, K., Izumiyama‐Shimomura, N., Honma, N., Sawabe, M., Arai, T., Kato, M., Oshimura, M., & Nakamura, K. (2002) · Experimental Gerontology · doi:10.1016/s0531-5565(01)00218-2 · Cited by 326 · see citing works
Inflammation, Glutamate, and Glia in Depression:<i>A Literature Review</i>
McNally, L., Bhagwagar, Z., & Hannestad, J. (2008) · CNS Spectrums · doi:10.1017/s1092852900016734 · Cited by 289 · see citing works
Telomere Biology and Cardiovascular Disease
Fuster, J. J., & Andrés, V. (2006) · Circulation Research · doi:10.1161/01.res.0000251281.00845.18 · Cited by 237 · see citing works
Rapid telomere erosion in schizophrenia
Kao, H.-T., Cawthon, R. M., DeLisi, L. E., Bertisch, H. C., Ji, F., Gordon, D., Li, P., Benedict, M. M., Greenberg, W. M., & Porton, B. (2008) · Molecular Psychiatry · doi:10.1038/sj.mp.4002105 · Cited by 128 · see citing works
DNA damage responses in neural cells: Focus on the telomere
Zhang, P., Dilley, C. M., & Mattson, M. P. (2007) · Neuroscience · doi:10.1016/j.neuroscience.2006.11.052 · Cited by 103 · see citing works
Cheng, A., Shin‐ya, K., Wan, R., Tang, S., Miura, T., Tang, H., Khatri, R. G., Gleichman, M., Ouyang, X., Liu, D., et al. (2007) · Journal of Neuroscience · doi:10.1523/jneurosci.0590-07.2007 · Cited by 75 · see citing works
Nakamura, K., Takubo, K., Izumiyama‐Shimomura, N., Sawabe, M., Arai, T., Kishimoto, H., Fujiwara, M., Kato, M., Oshimura, M., Ishii, A., et al. (2007) · Experimental Gerontology · doi:10.1016/j.exger.2007.05.003 · Cited by 63 · see citing works
Accumulation of oxidatively generated DNA damage in the brain: A mechanism of neurotoxicity
Chen, L., Lee, H. M., Greeley, G. H., & Englander, E. W. (2006) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2006.11.009 · Cited by 32 · see citing works
Wolkowitz, O. M., Epel, E. S., & Mellon, S. H. (2008) · The World Journal of Biological Psychiatry · doi:10.1080/15622970701875601 · Cited by 24 · see citing works
The applications of computers to research on nucleic acids
Bishop, M. J. (1982) · Trends in Biochemical Sciences · doi:10.1016/0968-0004(82)90272-9 · Cited by 13 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
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., et al. (2015) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2015.05.007 · Cited by 285 · see citing works
- 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