Evidence map›Paper›PMID 25726852›Full record

ArticleBipolar disorders2015

Prevalence of Huntington's disease gene CAG trinucleotide repeat alleles in patients with bipolar disorder.

Eliana Marisa Ramos, Tammy Gillis, Jayalakshmi S Mysore, Jong-Min Lee, Isabel Alonso, James F Gusella, Jordan W Smoller, Pamela Sklar, Marcy E MacDonald, Roy H Perlis

Open access · greenAbstract readComparative Study
In one paragraph

Article in Bipolar disorders, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. The Rich World of p53 DNA Binding Targets: The Role of DNA Structure.International journal of molecular sciences · 2019
    Review
  3. Review
  4. Haplotype-based stratification of Huntington's disease.European journal of human genetics : EJHG · 2017
    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

10 authors at 3 institutions in 2 countries.

Eliana Marisa RamosCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
Tammy GillisCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
Jayalakshmi S MysoreCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
Jong-Min LeeCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
Isabel AlonsoUnIGENe, IBMC - Institute for Molecular and Cell Biology, University of Porto, Porto, Portugal.ORCID http://orcid.org/0000-0001-8549-6903
James F GusellaCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
Jordan W SmollerCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
Pamela SklarDivision of Psychiatric Genomics, Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA.
Marcy E MacDonaldCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
Roy H PerlisCenter for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
Massachusetts General Hospital · USUniversidade do Porto · PTIcahn School of Medicine at Mount Sinai · US

Funding

TOXICITY AND SPECIFICITY COMPONENTS OF HD PATHOGENESISP50NS016367 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MACDONALD, MARCY · 1996 to 2010
$15.8M
GENETIC MODEL OF HUNTINGTONS DISEASER01NS032765 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MACDONALD, MARCY · 1994 to 2011
$3.7M
Building a Risk Stratification Model for Treatment Resistance in Major DepressiveR01MH086026 · NIMH · MASSACHUSETTS GENERAL HOSPITAL · PI PERLIS, ROY H. · 2009 to 2011
$1.3M
RECEPTOR MECHANISMS IN STRIATAL DEVELOPMENT AND HUNTINGTON'S DISEASEP01NS016367 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GUSELLA, JAMES F · 1985 to 1995
–
NIMH NIH HHS R01 MH086026NIMH NIH HHS R01MH086026NINDS NIH HHS NINDS NS16367NINDS NIH HHS NS32765NINDS NIH HHS P50 NS016367NINDS NIH HHS R01 NS032765
6 · The paper itself

Abstract

objectivesHuntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene (HTT) CAG trinucleotide repeat alleles of 36 or more units. A greater than expected prevalence of incompletely penetrant HTT CAG repeat alleles observed among individuals diagnosed with major depressive disorder raises the possibility that another mood disorder, bipolar disorder, could likewise be associated with Huntington's disease.

methodsWe assessed the distribution of HTT CAG repeat alleles in a cohort of individuals with bipolar disorder. HTT CAG allele sizes from 2,229 Caucasian individuals diagnosed with DSM-IV bipolar disorder were compared to allele sizes in 1,828 control individuals from multiple cohorts.

resultsWe found that HTT CAG repeat alleles > 35 units were observed in only one of 4,458 chromosomes from individuals with bipolar disorder, compared to three of 3,656 chromosomes from control subjects.

conclusionsThese findings do not support an association between bipolar disorder and Huntington's disease.

Indexed as

AdultAllelesAmyotrophic Lateral SclerosisBipolar DisorderFemaleGenotypeHumansHuntingtin ProteinHuntington DiseaseMajor Depressive DisorderMaleMiddle AgedNerve Tissue ProteinsPenetrancePrevalenceStatistics as TopicHTT protein, humanHuntingtin ProteinNerve Tissue Proteinsbipolar disorderdepressionHuntington's diseaseneurodegenerative diseasepolyglutamine expansiontrinucleotide repeat

Identifiers

PMID25726852
PMCPMC9980711
OpenAlexW2168231926

What OpenQuestion holds

Textmetadata
LicenceTDM
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.