Evidence map›Paper›PMID 23407780›Full record

ArticlePsychopharmacology2013

Screening genetic variability at the CNR1 gene in both major depression etiology and clinical response to citalopram treatment.

Marina Mitjans, Alessandro Serretti, Chiara Fabbri, Cristóbal Gastó, Rosa Catalán, Lourdes Fañanás, Bárbara Arias

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 4 pooled it
4.1field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 4 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. The American journal of drug and alcohol abuse · 2019
    Trial
  6. Molecular Changes Associated with Suicide.International journal of molecular sciences · 2023
    Review
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  11. Article
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  13. Cannabis and Depression.Advances in experimental medicine and biology · 2021
    Review
  14. Review
  15. Review
  16. Association of a Variant ofFrontiers in genetics · 2020
    Article
  17. Article
  18. Article
  19. Selective up-regulation of cannabinoid CBBiochemical pharmacology · 2018
    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

7 authors at 4 institutions in 2 countries.

Marina MitjansUnitat d'Antropologia, Departament de Biologia Animal, Facultat de Biologia, Universitat de Barcelona/Institut de Biomedicina de la Universitat de Barcelona (IBUB), Av. Diagonal, 643 2on pis, 08028 Barcelona, Spain.
Alessandro Serretti
Chiara Fabbri
Cristóbal Gastó
Rosa Catalán
Lourdes Fañanás
Bárbara Arias
Hospital Clínic de Barcelona · ESUniversitat de Barcelona · ESUniversity of Bologna · ITCentro de Investigación Biomédica en Red de Salud Mental · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleThe endocannabinoid system has been implicated in the pathogenesis of major depression (MD) as well as in the mediation of antidepressant drug effects.

objectivesTo analyze CNR1 gene variants in MD and clinical response to citalopram (selective serotonin re-uptake inhibitors [SSRI]).

methodsThe role of CNR1 gene (rs806368, rs1049353, rs806371, rs806377 and rs1535255) was investigated in 319 outpatients with MD and 150 healthy individuals. A subsample of 155 depressive patients were treated with citalopram and evaluated for response (fourth week) and remission (12th week) by the 21-item Hamilton Depression Rating Scale (HDRS).

resultsWe observed a higher frequency of rs806371 G carriers in MD patients with both presence of melancholia (p = 0.018) and psychotic symptoms (p = 0.007) than in controls. Haplotype frequency distributions between MD sample and controls showed a significant difference for Block 1 (rs806368-rs1049353-rs806371) (p = 0.008). This haplotype finding was consistent when we compared controls with MD subsample stratified by melancholia (p = 0.0009) and psychotic symptoms (p = 0.014). The TT homozygous of the rs806368 and rs806371 presented more risk of no Remission than the C carriers (p = 0.008 and 0.012, respectively). Haplotype frequency distributions according to Remission status showed a significant difference for Block 1 (p = 0.032). Also, we observed significant effect of time-sex-genotype interaction for the rs806368, showing that the C carrier men presented a better response to antidepressant treatment throughout the follow-up than TT homozygous men and women group (p = 0.026).

conclusionsThese results suggest an effect of CNR1 gene in the etiology of MD and clinical response to citalopram.

Indexed as

Polymorphism, Single NucleotideCase-Control StudiesCitalopramFemaleGene FrequencyHaplotypesHumansMajor Depressive DisorderMaleMiddle AgedPsychiatric Status Rating ScalesReceptor, Cannabinoid, CB1Risk FactorsSelective Serotonin Reuptake InhibitorsTreatment OutcomeCitalopramCNR1 protein, humanReceptor, Cannabinoid, CB1Selective Serotonin Reuptake Inhibitors

Identifiers

PMID23407780
OpenAlexW2024506145

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.