Evidence map›Paper›PMID 20159340›Full record

ReviewThe Psychiatric clinics of North America2010

Genetic research into bipolar disorder: the need for a research framework that integrates sophisticated molecular biology and clinically informed phenotype characterization.

Thomas G Schulze

Abstract readReview
In one paragraph

Review in The Psychiatric clinics of North America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

16 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Neural correlates of hallucinations in bipolar disorder.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2016
    Article
  3. Article
  4. Molecular actions and clinical pharmacogenetics of lithium therapy.Pharmacology, biochemistry, and behavior · 2014
    Review
  5. Molecular genetic overlap in bipolar disorder, schizophrenia, and major depressive disorder.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2014
    Article
  6. Article
  7. Diagnosing bipolar disorders in DSM-5.International journal of bipolar disorders · 2013
    Article
  8. Maternal perspectives on the return of genetic results: context matters.American journal of medical genetics. Part A · 2013
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Cognitive dysfunction is worse among pediatric patients with bipolar disorder Type I than Type II.Journal of child psychology and psychiatry, and allied disciplines · 2012
    Article
  14. Response to treatment in bipolar disorder.Current opinion in psychiatry · 2011
    Review
  15. Article
  16. Serum BDNF levels in unaffected first-degree relatives of patients with bipolar disorder.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999)
    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

1 author at 1 institution in 2 countries.

Thomas G SchulzeUnit on the Genetic Basis of Mood and Anxiety Disorders, National Institute of Mental Health (NIMH), National Institutes of Health (NIH), Bethesda, MD 20892-3719, USA. schulzet@mail.nih.gov
National Institute of Mental Health · US

Funding

Intramural NIH HHS Z99 MH999999
6 · The paper itself

Abstract

Research into the genetic basis of bipolar disorder (BD) has reached a turning point. Genome-wide association studies (GWAS), encompassing several thousand samples, have produced replicated evidence for some novel susceptibility genes; however, the genetic variants implicated so far account for only a fraction of disease liability, a phenomenon not limited to psychiatric phenotypes but characteristic of all complex genetic traits studied to date. It appears that pure genomic approaches, such as GWAS alone, will not suffice to unravel the genetic basis of a complex illness like BD. Genomic approaches will need to be complemented by a variety of strategies, including phenomics, epigenomics, pharmacogenomics, and neurobiology, as well as the study of environmental factors. This review highlights the most promising findings from recent GWAS and candidate gene studies in BD. It furthermore sketches out a potential research framework integrating various lines of research into the molecular biological basis of BD.

Indexed as

PhenotypeBipolar DisorderDepressive DisorderGene ExpressionGenetic LinkageGenome-Wide Association StudyGenotypeHumansMolecular BiologySchizophrenia

Identifiers

PMID20159340
PMCPMC2824617
OpenAlexW2016764740

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.