Evidence map›Paper›PMID 39208769›Full record

ArticleSchizophrenia research2024

Telomere biology and its maintenance in schizophrenia spectrum disorders: Exploring links to cognition.

Vid Mlakar, Ibrahim Akkouh, Els F Halff, Deepak P Srivastava, Viktoria Birkenæs, Torill Ueland, Daniel S Quintana, Monica B E G Ormerod, Nils Eiel Steen, Srdjan Djurovic and 2 more

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In one paragraph

Article in Schizophrenia research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Observational
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

12 authors.

Vid MlakarSocial, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. Electronic address: vid.2.mlakar@kcl.ac.uk.
Ibrahim AkkouhDepartment of Medical Genetics, Oslo University Hospital, Oslo, Norway; Centre for Precision Psychiatry, Division of Mental Health and Addiction, University of Oslo, Norway.
Els F HalffSocial, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Deepak P SrivastavaDepartment of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; MRC Centre for Neurodevelopmental Disorders, King's College London, London, UK.
Viktoria BirkenæsCentre for Precision Psychiatry, Division of Mental Health and Addiction, University of Oslo, Norway.
Torill UelandSection for Clinical Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital, Norway; Department of Psychology, University of Oslo, Oslo, Norway.
Daniel S QuintanaDepartment of Psychology, University of Oslo, Oslo, Norway; NevSom, Department of Rare Disorders, Oslo University Hospital, Oslo, Norway.
Monica B E G OrmerodSection for Clinical Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital, Norway.
Nils Eiel SteenCentre for Precision Psychiatry, Division of Mental Health and Addiction, University of Oslo, Norway; Section for Clinical Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital, Norway; Division of Mental Health and Substance Abuse, Diakonhjemmet Hospital, Oslo, Norway.
Srdjan DjurovicDepartment of Medical Genetics, Oslo University Hospital, Oslo, Norway; Department of Clinical Science, University of Bergen, Bergen, Norway.
Ole A AndreassenCentre for Precision Psychiatry, Division of Mental Health and Addiction, University of Oslo, Norway.
Monica AasSocial, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Department of Psychosis Studies, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, England, UK.

Funding

EU Framework Programme for Research and Innovation H2020 964874MRC MR/W027720/1Research Council of Norway 223273
6 · The paper itself

Abstract

objectiveContemporary research suggests reduced telomere length in schizophrenia spectrum disorders (SZ) compared to age-adjusted non-affected individuals. However, the role of telomere maintenance and telomere repair in SZ is poorly understood as well as the involvement of telomere biology in cognitive abnormalities in SZ.

methodsThe study consisted of 758 participants (SZ [n = 357] and healthy controls, HC [n = 401]) collected as part of the Norwegian TOP study. Participants were assessed with standardized neuropsychological tests measuring five cognitive domains. Leucocyte telomere length (TL) was measured via blood and determined by quantitative real-time Polymerase Chain Reaction (qPCR) providing a telomere to single copy ratio (T/S ratio), used to estimate the mean telomere length. Telomerase activity was assessed by the expression levels of the Telomerase Reverse Transcriptase (TERT) and Telomerase RNA Component (TERC) genes. To assess telomere maintenance and telomere repair we calculated the telomerase expression to TL ratio (TERT/TL and TERC/TL respectively).

resultsPatients had reduced TERT (F = 5.03, p = 0.03), but not TERC expression (F = 1.04, p = 0.31), and higher TERT/TL (F = 6.68, p = 0.01) and TERC/TL (F = 6.71, p = 0.01), adjusted for age, sex, and ethnicity. No statistically significant association was observed between any of the telomere biology markers and the cognitive domains (p > 0.05).

conclusionOur study shows changes in TERT expression and telomere maintenance and telomere repair in SZ compared HC. However, the role of telomere biology in the mechanism underlying cognitive impairment in psychosis seems limited.

Indexed as

SchizophreniaTelomeraseTelomereAdultCognitive DysfunctionFemaleHumansLeukocytesMaleMiddle AgedNeuropsychological TestsPsychotic DisordersRNASchizophrenic PsychologyTelomere HomeostasisTelomere ShorteningRNATelomerasetelomerase RNATERT protein, humanCognitive impairmentsSchizophrenia spectrum disordersTelomerase expressionTelomeres/telomere length maintenance and repair

Identifiers

PMID39208769
PMCPMC11846775

What OpenQuestion holds

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Registered trials

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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.