Evidence map›Paper›PMID 25826113›Full record

ArticleTranslational psychiatry2015

RNA expression profiling in depressed patients suggests retinoid-related orphan receptor alpha as a biomarker for antidepressant response.

J M Hennings, M Uhr, T Klengel, P Weber, B Pütz, C Touma, D Czamara, M Ising, F Holsboer, S Lucae

Abstract read
In one paragraph

Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 3 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

27 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Changes in RNA expression levels during antidepressant treatment: a systematic review.Journal of neural transmission (Vienna, Austria : 1996) · 2021
    Pooled it
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  18. Blood-based biomarkers predicting response to antidepressants.Journal of neural transmission (Vienna, Austria : 1996) · 2019
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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

10 authors.

J M HenningsDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
M UhrCore Unit Biobanking and Molecular Biology, Max Planck Institute of Psychiatry, Munich, Germany.
T KlengelDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
P WeberDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
B PützDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
C ToumaDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
D CzamaraDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
M IsingDepartment of Clinical Research, Max Planck Institute of Psychiatry, Munich, Germany.
F HolsboerEmeritus scientific member, Max Planck Institute of Psychiatry, Munich, Germany.
S LucaeDepartment of Clinical Research, Max Planck Institute of Psychiatry, Munich, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Response to antidepressant treatment is highly variable with some patients responding within a few weeks, whereas others have to wait for months until the onset of clinical effects. Gene expression profiling may be a tool to identify markers of antidepressant treatment response and new potential drug targets. In a first step, we selected 12 male, age- and severity-matched pairs of remitters and nonresponders, and analyzed expression profiles in peripheral blood at admission and after 2 and 5 weeks of treatment using Illumina expression arrays. We identified 127 transcripts significantly associated with treatment response with a minimal P-value of 9.41 × 10(-)(4) (false discovery rate-corrected). Analysis of selected transcripts in an independent replication sample of 142 depressed inpatients confirmed that lower expression of retinoid-related orphan receptor alpha (RORa, P=6.23 × 10(-4)), germinal center expressed transcript 2 (GCET2, P=2.08 × 10(-2)) and chitinase 3-like protein 2 (CHI3L2, P=4.45 × 10(-2)) on admission were associated with beneficial treatment response. In addition, leukocyte-specific protein 1 (LSP1) significantly decreased after 5 weeks of treatment in responders (P=2.91 × 10(-2)). Additional genetic, in vivo stress responsitivity data and murine gene expression findings corroborate our finding of RORa as a transcriptional marker of antidepressant response. In summary, using a genome-wide transcriptomics approach and subsequent validation studies, we identified several transcripts including the circadian gene transcript RORa that may serve as biomarkers indicating antidepressant treatment response.

Indexed as

AdultAnimalsAntidepressive AgentsDepressive DisorderDisease Models, AnimalFollow-Up StudiesGene Expression ProfilingGenetic MarkersHumansMaleMiceMiddle AgedNuclear Receptor Subfamily 1, Group F, Member 1RNATreatment OutcomeAntidepressive AgentsGenetic MarkersNuclear Receptor Subfamily 1, Group F, Member 1RNA

Identifiers

PMID25826113
PMCPMC4429173

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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.