Evidence map›Paper›PMID 25618407›Full record

ArticleThe international journal of neuropsychopharmacology2015

Telomerase dysregulation in the hippocampus of a rat model of depression: normalization by lithium.

Ya Bin Wei, Lena Backlund, Gregers Wegener, Aleksander A Mathé, Catharina Lavebratt

Open access · goldAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 4 pooled it
5.2field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 4 syntheses or guidelines pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Meta-analysis of Telomere Length in Alzheimer's Disease.The journals of gerontology. Series A, Biological sciences and medical sciences · 2016
    Pooled it
  5. PBMC telomerase activity in depression and the response to electroconvulsive therapy.European archives of psychiatry and clinical neuroscience · 2021
    Trial
  6. Trial
  7. Article
  8. Review
  9. The Mechanisms of Lithium Action: The Old and New Findings.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Cellular Senescence in Brain Aging.Frontiers in aging neuroscience · 2021
    Review
  16. Article
  17. Article
  18. Review
  19. Telomere Biology in Mood Disorders: An Updated, Comprehensive Review of the Literature.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2019
    Article
  20. Article
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

5 authors at 3 institutions in 3 countries.

Ya Bin WeiDepartment of Molecular Medicine and Surgery, Neurogenetics Unit, Karolinska Institutet, Stockholm, Sweden (Mr Wei, Drs Backlund and Lavebratt); Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden (Mr Wei, Dr Lavebratt); Centre for Psychiatric Research and Education, Karolinska Institutet, Clinic for Affective Disorders, Stockholm, Sweden (Drs Backlund and Mathé); Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark (Dr Wegener); Centre of Excellence for Pharmaceutical Sciences, North-West University, Potchefstroom, South Africa (Dr Wegener); and Department of Clinical Neuroscience, Section for Psychiatry, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Lena BacklundDepartment of Molecular Medicine and Surgery, Neurogenetics Unit, Karolinska Institutet, Stockholm, Sweden (Mr Wei, Drs Backlund and Lavebratt); Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden (Mr Wei, Dr Lavebratt); Centre for Psychiatric Research and Education, Karolinska Institutet, Clinic for Affective Disorders, Stockholm, Sweden (Drs Backlund and Mathé); Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark (Dr Wegener); Centre of Excellence for Pharmaceutical Sciences, North-West University, Potchefstroom, South Africa (Dr Wegener); and Department of Clinical Neuroscience, Section for Psychiatry, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Gregers WegenerDepartment of Molecular Medicine and Surgery, Neurogenetics Unit, Karolinska Institutet, Stockholm, Sweden (Mr Wei, Drs Backlund and Lavebratt); Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden (Mr Wei, Dr Lavebratt); Centre for Psychiatric Research and Education, Karolinska Institutet, Clinic for Affective Disorders, Stockholm, Sweden (Drs Backlund and Mathé); Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark (Dr Wegener); Centre of Excellence for Pharmaceutical Sciences, North-West University, Potchefstroom, South Africa (Dr Wegener); and Department of Clinical Neuroscience, Section for Psychiatry, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Aleksander A MathéDepartment of Molecular Medicine and Surgery, Neurogenetics Unit, Karolinska Institutet, Stockholm, Sweden (Mr Wei, Drs Backlund and Lavebratt); Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden (Mr Wei, Dr Lavebratt); Centre for Psychiatric Research and Education, Karolinska Institutet, Clinic for Affective Disorders, Stockholm, Sweden (Drs Backlund and Mathé); Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark (Dr Wegener); Centre of Excellence for Pharmaceutical Sciences, North-West University, Potchefstroom, South Africa (Dr Wegener); and Department of Clinical Neuroscience, Section for Psychiatry, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Catharina LavebrattDepartment of Molecular Medicine and Surgery, Neurogenetics Unit, Karolinska Institutet, Stockholm, Sweden (Mr Wei, Drs Backlund and Lavebratt); Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden (Mr Wei, Dr Lavebratt); Centre for Psychiatric Research and Education, Karolinska Institutet, Clinic for Affective Disorders, Stockholm, Sweden (Drs Backlund and Mathé); Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark (Dr Wegener); Centre of Excellence for Pharmaceutical Sciences, North-West University, Potchefstroom, South Africa (Dr Wegener); and Department of Clinical Neuroscience, Section for Psychiatry, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Aarhus University · DKKarolinska Institutet · SENorth-West University · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTelomeres are protective DNA-protein complexes at the ends of each chromosome, maintained primarily by the enzyme telomerase. Shortening of the blood leukocyte telomeres is associated with aging, several chronic diseases, and stress, eg, major depression. Hippocampus is pivotal in the regulation of cognition and mood and the main brain region of telomerase activity. Whether there is telomere dysfunction in the hippocampus of depressed subjects is unknown. Lithium, used in the treatment and relapse prevention of mood disorders, was found to protect against leukocyte telomere shortening in humans, but the mechanism has not been elucidated. To answer the questions whether telomeres are shortened and the telomerase activity changed in the hippocampus and whether lithium could reverse the process, we used a genetic model of depression, the Flinders Sensitive Line rat, and treated the animals with lithium.

methodsTelomere length, telomerase reverse transcriptase (Tert) expression, telomerase activity, and putative mediators of telomerase activity were investigated in the hippocampus of these animals.

resultsThe naïve Flinders Sensitive Line had shorter telomere length, downregulated Tert expression, reduced brain-derived neurotrophic factor levels, and reduced telomerase activity compared with the Flinders Resistant Line controls. Lithium treatment normalized the Tert expression and telomerase activity in the Flinders Sensitive Line and upregulated β-catenin.

conclusionThis is the first report showing telomere dysregulation in hippocampus of a well-defined depression model and restorative effects of lithium treatment. If replicated in other models of mood disorder, the findings will contribute to understanding both the telomere function and the mechanism of lithium action in hippocampus of depressed patients.

Indexed as

AgingAnimalsAntidepressive AgentsBehavior, Animalbeta CateninBrain-Derived Neurotrophic FactorDepressionDisease Models, AnimalHippocampusLithium CompoundsMaleRatsRats, Inbred StrainsTelomeraseTelomereTreatment OutcomeAntidepressive Agentsbeta CateninBrain-Derived Neurotrophic FactorLithium CompoundsTelomeraseanimal modeldepressionhippocampuslithiumtelomerasetelomere

Identifiers

PMID25618407
PMCPMC4540104
OpenAlexW2111096670

What OpenQuestion holds

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LicenceCC BY
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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.