Evidence map›Paper›PMID 19829169›Full record

ArticlePsychiatric genetics2009

SSRI response in depression may be influenced by SNPs in HTR1B and HTR1A.

Sandra M Villafuerte, Kamala Vallabhaneni, Elzbieta Sliwerska, Francis J McMahon, Elizabeth A Young, Margit Burmeister

Abstract read
In one paragraph

Article in Psychiatric genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 20% 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, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Bone Turnover with Venlafaxine Treatment in Older Adults with Depression.Journal of the American Geriatrics Society · 2017
    Trial
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  6. Unmet needs in precision psychiatry.World journal of psychiatry · 2025
    Article
  7. Article
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  9. Review
  10. Article
  11. Article
  12. Blood-based biomarkers predicting response to antidepressants.Journal of neural transmission (Vienna, Austria : 1996) · 2019
    Review
  13. Cognitive Control as a 5-HTFrontiers in psychology · 2019
    Article
  14. The 5-HTPsychopharmacology · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

6 authors at 2 institutions in 2 countries.

Sandra M VillafuerteMolecular & Behavioral Neuroscience Institute, Department of Psychiatry, University of Michigan, Ann Arbor, Michigan 48109-2200, USA. svillafu@umich.edu
Kamala Vallabhaneni
Elzbieta Sliwerska
Francis J McMahon
Elizabeth A Young
Margit Burmeister
Neuroscience Institute · ITNational Institutes of Health · US

Funding

Genetic Determinants of Antidepressant Response in the STAR*D CohortZIAMH002844 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI MCMAHON, FRANCIS J · 2009 to 2025
$11.1M
Genetic Determinants of Antidepressant Response STAR*DZ01MH002844 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI MCMAHON, FRANCIS J · 2004 to 2008
$832k
Intramural NIH HHS Z01 MH002844
6 · The paper itself

Abstract

objectivesDesensitization of serotonin 1A (HTR1A) and 1B (HTR1B) autoreceptors has been proposed to be involved in the delayed onset of response to selective serotonin reuptake inhibitors (SSRIs). Variations in gene expression in these genes may thus affect SSRI response.

methodsHere, we test this hypothesis in two samples from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D), and show evidence for involvement of several genetic variants alone and in interaction. Initially, three functional single nucleotide polymorphisms (SNPs) in the HTR1B gene and in the HTR1A gene were analyzed in 153 depressed patients treated with citalopram. The 16-item Quick Inventory of Depressive Symptomatology Clinician scores were evaluated over time with respect to genetic variation.

resultsIndividuals homozygous for the -1019 G allele (rs6295) in HTR1A showed the higher baseline 16-item Quick Inventory of Depressive Symptomatology Clinician scores (P=0.033), and by 12 weeks had a significantly lower response rate (P=0.005). HTR1B haplotypes were estimated according to the previously reported in-vitro expression levels. Individuals who were homozygous for the high-expression haplotype showed significantly slower response to citalopram (P=0.034). We then analyzed more SNPs in the extended overall STAR*D sample. Although we could not directly test the same functional SNPs, we found that homozygotes for the G allele at rs1364043 in HTR1A (P=0.045) and the C allele of rs6298 in HTR1B showed better response to citalopram over time (P=0.022). Test for interaction between rs6298 in HTR1B and rs1364043 in HTR1A was significant (overall P=0.032).

conclusionOur data suggest that an enhanced capacity of HTR1B or HTR1A transcriptional activity may impair desensitization of the autoreceptors during SSRI treatment.

Indexed as

Polymorphism, Single NucleotideDepressionHumansReceptor, Serotonin, 5-HT1AReceptor, Serotonin, 5-HT1BSelective Serotonin Reuptake InhibitorsReceptor, Serotonin, 5-HT1AReceptor, Serotonin, 5-HT1BSelective Serotonin Reuptake Inhibitors

Identifiers

PMID19829169
PMCPMC2783179
OpenAlexW2059815221

What OpenQuestion holds

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Read underepoch 390

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.