Evidence map›Paper›PMID 16914640›Full record

ReviewSchizophrenia bulletin2006

The G72/G30 gene locus in psychiatric disorders: a challenge to diagnostic boundaries?

Rami Abou Jamra, Christine Schmael, Sven Cichon, Marcella Rietschel, Johannes Schumacher, Markus M Nöthen

Open access · bronzeAbstract readReview
In one paragraph

Review in Schizophrenia bulletin, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Beyond Depression: Towards a Process-Based Approach to Research, Diagnosis, and Treatment.Clinical psychology : a publication of the Division of Clinical Psychology of the American Psychological Association · 2011
    Article
  3. N-acetyl cysteine treatment rescues cognitive deficits induced by mitochondrial dysfunction in G72/G30 transgenic mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
    Article
  4. Article
  5. Article
  6. Searching for valid psychiatric phenotypes: discrete latent variable models.International journal of methods in psychiatric research · 2010
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. 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 3 institutions in 1 country.

Rami Abou JamraInstitute of Human Genetics, University of Bonn, Wilhelmstrasse 31, D-53111 Bonn, Germany. rami.aboujamra@uni-bonn.de
Christine Schmael
Sven Cichon
Marcella Rietschel
Johannes Schumacher
Markus M Nöthen
University of Bonn · DECentral Institute of Mental Health · DELife & Brain (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In follow-up from evidence obtained in linkage studies, systematic linkage disequilibrium mapping within chromosomal region 13q33 has led to the identification of a schizophrenia susceptibility locus which harbors the genes G72 and G30. These association findings have been replicated in several independent schizophrenia samples. Association has also been found between genetic variants at the G72/G30 locus and bipolar affective disorder (BPAD), with replication in independent studies. Results from studies of more detailed psychiatric phenotypes show that association exists with symptom clusters that are common to several disorders as well as with specific psychiatric diagnoses. These findings may indicate that the association lies not with the diagnostic categories per se but with more specific aspects of the phenotype, such as affective symptoms and cognitive effects, which cross traditional psychiatric diagnostic boundaries. At the molecular level, the picture remains far from clear. No putative functional variants have been identified in the coding regions of G72 or G30, and it is therefore likely that disease susceptibility is caused by as yet unidentified variants which alter gene expression or splicing. A further complication is the fact that inconsistencies are evident in the risk alleles and haplotypes observed to be associated across different samples and studies, which may suggest the presence of multiple susceptibility variants at this locus. Functional analyses indicate that the G72 gene product plays a role in the activation of N-methyl-D-aspartate receptors, a molecular pathway implicated in both schizophrenia and BPAD, making it the most plausible candidate gene at this locus.

Indexed as

Bipolar DisorderCarrier ProteinsChromosome MappingGene ExpressionGenetic Predisposition to DiseaseGenetic VariationGenotypeIntracellular Signaling Peptides and ProteinsLinkage DisequilibriumProteinsQuantitative Trait LociReceptors, N-Methyl-D-AspartateRNA, MessengerSchizophreniaCarrier ProteinsDAOAAS gene product, humanDAOA protein, humanIntracellular Signaling Peptides and ProteinsProteinsReceptors, N-Methyl-D-AspartateRNA, Messenger

Identifiers

PMID16914640
PMCPMC2632259
OpenAlexW2109629603

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.