Evidence map›Paper›PMID 25793616›Full record

ArticlePloS one2015

COMT and MAO-A polymorphisms and obsessive-compulsive disorder: a family-based association study.

Aline Santos Sampaio, Ana Gabriela Hounie, Kátia Petribú, Carolina Cappi, Ivanil Morais, Homero Vallada, Maria Conceição do Rosário, S Evelyn Stewart, Jesen Fargeness, Carol Mathews and 8 more

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

3 citing papers in PubMed, 23 citations in OpenAlex.

  1. Pharmacotherapeutic Strategies and New Targets in OCD.Current topics in behavioral neurosciences · 2021
    Review
  2. Article
  3. 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

18 authors at 12 institutions in 3 countries.

Aline Santos SampaioDepartment and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil; Serviço Médico Universitário, Universidade Federal da Bahia (UFBA, Federal University of Bahia), Salvador, BA, Brazil.
Ana Gabriela HounieDepartment and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
Kátia PetribúUniversidade de Pernambuco (UPE, University of Pernambuco) Faculdade de Ciências Médicas, Recife, PE, Brazil.
Carolina CappiDepartment and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
Ivanil MoraisDepartment and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
Homero ValladaDepartment and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
Maria Conceição do RosárioUniversidade Federal de Sao Paulo (UNIFESP, Federal University of São Paulo), São Paulo, SP, Brazil.
S Evelyn StewartBritish Columbia Mental Health and Addictions Research Institute, Vancouver, BC, Canada; Psychiatric and Neurodevelopmental Genetics Unit (PNGU), Massachusetts General Hospital, Boston, Massachusetts, United States of America.
Jesen FargenessCenter for Human Genetics Research, Massachusetts General Hospital, Boston, Massachusetts, United States of America.
Carol MathewsDepartment of Psychiatry, University of California, San Francisco, California, United States of America.
Paul ArnoldProgram in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, Ontario, Canada.
Gregory L HannaDepartment of Psychiatry, University of Michigan, Ann Arbor, Michigan, United States of America.
Margaret RichterThe Frederick W. Thompson Anxiety Disorders Centre, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada.
James KennedyCentre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada.
Leonardo FontenellePrograma de Ansiedade e Depressão, Instituto de Psiquiatria, Universidade Federal do Rio de Janeiro (IPUB/UFRJ), Rio de Janeiro, RJ, Brazil.
Carlos Alberto de Bragança PereiraDepartment of Statistics, The Institute of Mathematics and Statistics, University of São Paulo, SP, Brazil.
David L PaulsPsychiatric and Neurodevelopmental Genetics Unit (PNGU), Massachusetts General Hospital, Boston, Massachusetts, United States of America.
Eurípedes Constantino MiguelDepartment and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRMassachusetts General Hospital · USCenter for Human Genetics · USHealth Sciences Centre · CAHospital for Sick Children · CAUniversidade de Pernambuco · BRUniversidade de São Paulo · BRUniversidade Federal de São Paulo · BRUniversidade Federal do Rio de Janeiro · BRUniversity of California, San Francisco · USUniversity of Michigan–Ann Arbor · USUniversity of Toronto · CA

Funding

2/3 Brain Function and Genetics in Pediatric Obsessive-Compulsive BehaviorsR01MH085321 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HANNA, GREGORY L. · 2009 to 2019
$2.9M
NIMH NIH HHS R01 MH085321
6 · The paper itself

Abstract

objectiveObsessive-compulsive disorder (OCD) is a common and debilitating psychiatric illness. Although a genetic component contributes to its etiology, no single gene or mechanism has been identified to the OCD susceptibility. The catechol-O-methyltransferase (COMT) and monoamine oxidase A (MAO-A) genes have been investigated in previous OCD studies, but the results are still unclear. More recently, Taylor (2013) in a comprehensive meta-analysis of genetic association studies has identified COMT and MAO-A polymorphisms involved with OCD. In an effort to clarify the role of these two genes in OCD vulnerability, a family-based association investigation was performed as an alternative strategy to the classical case-control design.

methodsTransmission disequilibrium analyses were performed after genotyping 13 single-nucleotide polymorphisms (eight in COMT and five in MAO-A) in 783 OCD trios (probands and their parents). Four different OCD phenotypes (from narrow to broad OCD definitions) and a SNP x SNP epistasis were also analyzed.

resultsOCD, broad and narrow phenotypes,were not associated with any of the investigated COMT and MAO-A polymorphisms. In addition, the analyses of gene-gene interaction did not show significant epistatic influences on phenotype between COMT and MAO-A.

conclusionsThe findings do not support an association between DSM-IV OCD and the variants of COMT or MAO-A. However, results from this study cannot exclude the contribution of these genes in the manifestation of OCD. The evaluation of broader spectrum phenotypes could help to understand the role of these and other genes in the pathophysiology of OCD and its spectrum disorders.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseasePolymorphism, Single NucleotideAdolescentAdultAllelesCatechol O-MethyltransferaseChildEpistasis, GeneticFamilyFemaleGene FrequencyGenotypeHaplotypesHumansLinkage DisequilibriumCatechol O-MethyltransferaseCOMT protein, humanMonoamine Oxidasemonoamine oxidase A, human

Identifiers

PMID25793616
PMCPMC4368617
OpenAlexW1977948482

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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.