Evidence map›Paper›PMID 27325393›Full record

ArticlePsychopharmacology2016

Molecular serum signature of treatment resistant depression.

Tillmann Ruland, Man K Chan, Pawel Stocki, Laura Grosse, Matthias Rothermundt, Jason D Cooper, Volker Arolt, Sabine Bahn

Abstract read
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Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

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  5. Telomere attrition and inflammatory load in severe psychiatric disorders and in response to psychotropic medications.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
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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

8 authors at 2 institutions in 2 countries.

Tillmann RulandMood and Anxiety Disorders Research Unit, Department of Psychiatry and Psychotherapy, University of Muenster, Muenster, Germany. Tillmann.Ruland@ukmuenster.de.
Man K ChanDepartment of Chemical Engineering and Biotechnology, University of Cambridge, Cambridge, UK.
Pawel StockiDepartment of Chemical Engineering and Biotechnology, University of Cambridge, Cambridge, UK.
Laura GrosseMood and Anxiety Disorders Research Unit, Department of Psychiatry and Psychotherapy, University of Muenster, Muenster, Germany.
Matthias RothermundtMood and Anxiety Disorders Research Unit, Department of Psychiatry and Psychotherapy, University of Muenster, Muenster, Germany.
Jason D CooperDepartment of Chemical Engineering and Biotechnology, University of Cambridge, Cambridge, UK.
Volker AroltMood and Anxiety Disorders Research Unit, Department of Psychiatry and Psychotherapy, University of Muenster, Muenster, Germany.
Sabine BahnDepartment of Chemical Engineering and Biotechnology, University of Cambridge, Cambridge, UK.
University of Cambridge · GBUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleA substantial number of patients suffering from major depressive disorder (MDD) do not respond to multiple trials of anti-depressants, develop a chronic course of disease and become treatment resistant. Most of the studies investigating molecular changes in treatment-resistant depression (TRD) have only examined a limited number of molecules and genes. Consequently, biomarkers associated with TRD are still lacking.

objectivesThis study aimed to use recently advanced high-throughput proteomic platforms to identify peripheral biomarkers of TRD defined by two staging models, the Thase and Rush staging model (TRM) and the Maudsley Staging Model (MSM).

methodsSerum collected from an inpatient cohort of 65 individuals suffering from MDD was analysed using two different mass spectrometric-based platforms, label-free liquid chromatography mass spectrometry (LC-MS(E)) and selective reaction monitoring (SRM), as well as a multiplex bead based assay.

resultsIn the LC-MS(E) analysis, proteins involved in the acute phase response and complement activation and coagulation were significantly different between the staging groups in both models. In the multiplex bead-based assay analysis TNF-α levels (log(odds) = -4.95, p = 0.045) were significantly different in the TRM comparison. Using SRM, significant changes of three apolipoproteins A-I (β = 0.029, p = 0.035), M (β = -0.017, p = 0.009) and F (β = -0.031, p = 0.024) were associated with the TRM but not the MSM.

conclusionOverall, our findings suggest that proteins, which are involved in immune and complement activation, may represent potential biomarkers that could be used by clinicians to identify high-risk patients. Nevertheless, given that the molecular changes between the staging groups were subtle, the results need to be interpreted cautiously.

Indexed as

ProteomicsAdultAntidepressive AgentsBiomarkersBlood CoagulationChromatography, LiquidCohort StudiesComplement ActivationCytokinesDepressive Disorder, Treatment-ResistantDNA Mismatch RepairFemaleHumansLogistic ModelsMajor Depressive DisorderMaleAntidepressive AgentsBiomarkersCytokinesTNF protein, humanTumor Necrosis Factor-alphaMass spectrometrySerumStagingTreatment resistant depression

Identifiers

PMID27325393
OpenAlexW2466185491

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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.