Evidence map›Paper›PMID 34291629›Full record

ArticleJournal of psychiatry & neuroscience : JPN2021

Alterations of cellular aging markers in obsessive- compulsive disorder: mitochondrial DNA copy number and telomere length.

Jee In Kang, Chun Il Park, Jue Lin, Shin Tae Kim, Hae Won Kim, Se Joo Kim

Open access · diamondAbstract read
In one paragraph

Article in Journal of psychiatry & neuroscience : JPN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Jee In KangFrom the Department of Psychiatry and Institute of Behavioural Science in Medicine, Yonsei University College of Medicine, Seoul, South Korea (Kang, S.-T. Kim, S.-J. Kim); the Department of Psychiatry, CHA Bundang Medical Centre, CHA University, Seongnam, Republic of Korea (Park); the Department of Biochemistry and Biophysics, UCSF School of Medicine, San Francisco, CA, USA (Lin); and the Department of Medical Education, Yonsei University College of Medicine, Seoul, South Korea (H.-W. Kim).
Chun Il ParkFrom the Department of Psychiatry and Institute of Behavioural Science in Medicine, Yonsei University College of Medicine, Seoul, South Korea (Kang, S.-T. Kim, S.-J. Kim); the Department of Psychiatry, CHA Bundang Medical Centre, CHA University, Seongnam, Republic of Korea (Park); the Department of Biochemistry and Biophysics, UCSF School of Medicine, San Francisco, CA, USA (Lin); and the Department of Medical Education, Yonsei University College of Medicine, Seoul, South Korea (H.-W. Kim).
Jue LinFrom the Department of Psychiatry and Institute of Behavioural Science in Medicine, Yonsei University College of Medicine, Seoul, South Korea (Kang, S.-T. Kim, S.-J. Kim); the Department of Psychiatry, CHA Bundang Medical Centre, CHA University, Seongnam, Republic of Korea (Park); the Department of Biochemistry and Biophysics, UCSF School of Medicine, San Francisco, CA, USA (Lin); and the Department of Medical Education, Yonsei University College of Medicine, Seoul, South Korea (H.-W. Kim).
Shin Tae KimFrom the Department of Psychiatry and Institute of Behavioural Science in Medicine, Yonsei University College of Medicine, Seoul, South Korea (Kang, S.-T. Kim, S.-J. Kim); the Department of Psychiatry, CHA Bundang Medical Centre, CHA University, Seongnam, Republic of Korea (Park); the Department of Biochemistry and Biophysics, UCSF School of Medicine, San Francisco, CA, USA (Lin); and the Department of Medical Education, Yonsei University College of Medicine, Seoul, South Korea (H.-W. Kim).
Hae Won KimFrom the Department of Psychiatry and Institute of Behavioural Science in Medicine, Yonsei University College of Medicine, Seoul, South Korea (Kang, S.-T. Kim, S.-J. Kim); the Department of Psychiatry, CHA Bundang Medical Centre, CHA University, Seongnam, Republic of Korea (Park); the Department of Biochemistry and Biophysics, UCSF School of Medicine, San Francisco, CA, USA (Lin); and the Department of Medical Education, Yonsei University College of Medicine, Seoul, South Korea (H.-W. Kim).
Se Joo KimFrom the Department of Psychiatry and Institute of Behavioural Science in Medicine, Yonsei University College of Medicine, Seoul, South Korea (Kang, S.-T. Kim, S.-J. Kim); the Department of Psychiatry, CHA Bundang Medical Centre, CHA University, Seongnam, Republic of Korea (Park); the Department of Biochemistry and Biophysics, UCSF School of Medicine, San Francisco, CA, USA (Lin); and the Department of Medical Education, Yonsei University College of Medicine, Seoul, South Korea (H.-W. Kim).
CHA University · KRCHA University Bundang Medical Center · KRUniversity of California, San Francisco · USYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe present study examined whether mitochondrial DNA copy number (mtDNAcn) and telomere length - key markers of cellular aging - were altered in male and female participants with obsessive-compulsive disorder (OCD) compared to healthy controls. We also tested for associations between these alterations and OCD-related clinical features and inflammatory index.

methodsA total of 235 patients with OCD (38.7% female) and 234 healthy controls (41.5% female) were included. We quantified whole-blood mtDNAcn and leukocyte telomere length using quantitative polymerase chain reaction. We also calculated the neutrophil-to-lymphocyte ratio from complete blood cell counts.

resultsMultivariate analysis of covariance showed that OCD status had a significant overall effect on cellular aging markers in men (Wilks λ = 0.889, F2,275 = 17.13, p < 0.001) and women (Wilks λ = 0.742, F2,182 = 31.61, p < 0.001) after controlling for age, body mass index and childhood trauma. In post-hoc comparisons, men with OCD had lower mtDNAcn than controls (p < 0.001), but we found no between-group difference for telomere length (p = 0.55). Women with OCD had a significantly lower mtDNAcn (p < 0.001) and shortened telomere length (p = 0.023) compared to controls. Moreover, the lower mtDNAcn shown in the OCD group was significantly correlated with an increase in systemic inflammation for both sexes, as measured by neutrophil-to-lymphocyte ratio. LIMITATIONS: The present cross-sectional design did not allow us to infer a causal relationship between OCD disease status and cellular aging markers.

conclusionThe present study is, to our knowledge, the first to demonstrate alterations in mtDNAcn and telomere shortening in OCD. These results suggest that aging-associated molecular mechanisms may be important in the pathophysiology of OCD.

Indexed as

AdultBiomarkersCellular SenescenceCross-Sectional StudiesDNA Copy Number VariationsDNA, MitochondrialFemaleHumansMaleMiddle AgedObsessive-Compulsive DisorderTelomereTelomere ShorteningYoung AdultBiomarkersDNA, Mitochondrial

Identifiers

PMID34291629
PMCPMC8519490
OpenAlexW3184752240

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.