Schizophrenia Research Forum - A Catalyst for Creative Thinking
Home Profile Membership/Get Newsletter Log In Contact Us
 For Patients & Families
What's New
Recent Updates
SRF Papers
Current Papers
Search All Papers
Search Comments
News
Research News
Conference News
Plain English
Forums
Current Hypotheses
Idea Lab
Online Discussions
Virtual Conferences
Interviews
Resources
What We Know
SchizophreniaGene
Animal Models
Drugs in Trials
Research Tools
Grants
Jobs
Conferences
Journals
Community Calendar
General Information
Community
Member Directory
Researcher Profiles
Institutes and Labs
About the Site
Mission
History
SRF Team
Advisory Board
Support Us
How to Cite
Fan (E)Mail
The Schizophrenia Research Forum web site is sponsored by the Brain and Behavior Research Foundation and was created with funding from the U.S. National Institute of Mental Health.
Annotation

Detera-Wadleigh SD, McMahon FJ. G72/G30 in schizophrenia and bipolar disorder: review and meta-analysis. Biol Psychiatry . 2006 Jul 15 ; 60(2):106-14. PubMed Abstract

Comments on Paper and Primary News
Comment by:  Michael Owen, SRF Advisor
Submitted 19 April 2006 Posted 19 April 2006

This is an excellent article that contains a meta-analysis of the putative association between G72/G30 with schizophrenia (SZ) and bipolar disorder (BP), together with a review of the relevant data from linkage and biology that place the association findings in context. I think that the authors are correct to conclude that, while the association data certainly favor the view that variation at this locus confers risk for both BP and SZ, a number of nagging concerns remain. The lack of consistency between the associated alleles in different studies could reflect true heterogeneity, but there are a number of artifactual causes that need to be excluded. Second, some of the best associated SNPs actually map some distance from the gene and in a different LD block to other associated SNPs. If both these sets of findings are correct, this also suggests that whatever is going on at the level of the gene is more complex than a simple association with a single functional variant. Third, no one has yet succeeded in demonstrating expression of the G72 protein. This might be...  Read more


View all comments by Michael Owen
Comments on Related News
Related News: Genetic Studies of DAOA(G72)/G30 Bridge Kraepelinian Divide

Comment by:  Patricia Estani
Submitted 23 April 2006 Posted 23 April 2006
  I recommend the Primary Papers

Related News: Genetic Studies of DAOA(G72)/G30 Bridge Kraepelinian Divide

Comment by:  Edward Scolnick
Submitted 23 April 2006 Posted 23 April 2006

I would caution that G72 has not been shown to be an actual gene, and in the four years since Chumakov and colleagues' report, the biochemistry has not been reproduced.

View all comments by Edward Scolnick


Related News: Genetic Studies of DAOA(G72)/G30 Bridge Kraepelinian Divide

Comment by:  Nick CraddockMichael Owen (SRF Advisor)
Submitted 26 April 2006 Posted 26 April 2006

Reply to comment by Dr Scolnick
We agree that caution is required regarding the assumption that the genetic association at this locus is causally related to the DAOA "gene," and this is the reason that in the paper we have referred to the "DAOA/ G30 locus." Establishing robust genetic association in a restricted region of the genome is clearly the first step on a path to characterizing the biological and phenotypic relationships associated with the variation. It is entirely possible that pathologically relevant variation occurs at the DAOA/G30 locus that does not involve a protein product of the DAOA DNA sequence.

View all comments by Nick Craddock
View all comments by Michael Owen


Related News: Genetic Studies of DAOA(G72)/G30 Bridge Kraepelinian Divide

Comment by:  Daniel Weinberger, SRF Advisor
Submitted 10 May 2006 Posted 10 May 2006

The DAOA/G30 locus is a paradigm of association in psychiatric genetics, where positive reports are followed by both confirmation of association and failures to associate, with the observers of the glass being half-full commenting that it is unlikely that replication would occur spuriously multiple times, and those seeing the glass as half-empty (or three-quarters empty) emphasizing allelic inconsistencies, lack of identified causative SNPs, and in the case of DAOA/G30, lack of conclusive evidence of a gene expressed in brain. Clearly, we are just scratching the surface of understanding the reasons for any association signal in this region of the genome. It is important to remember that the DAOA/G30 locus was cloned from a region that has shown linkage in a number of studies, giving prior probability to association analyses, and that association has been reported in samples from a number of corners of the world. Expression may be restricted to discrete times in development and may not be present in abundance in middle-aged brains. It is also possible, as noted by Mike Owen,...  Read more


View all comments by Daniel Weinberger
Submit a Comment on this Paper
Make a comment on this paper. 

If you already are a member, please login.
Not sure if you are a member? Search our member database.

*First Name  
*Last Name  
Affiliation  
Country or Territory  
*Login Email Address  
*Confirm Email Address  
*Password  
*Confirm Password  
Remember my Login and Password?  
Get SRF newsletter with recent commentary?  
 
Enter the code as it is shown below:
This code helps prevent automated registrations.

I recommend this paper

Please note: A member needs to be both registered and logged in to submit a comment.

Comment:

(If coauthors exist for this comment, please enter their names and email addresses at the end of the comment.)

References:


 
 
SRF News
SRF Comments
Text Size
Reset Text Size
Email this pageEmail this page

Share/Bookmark
 
Copyright © 2005- 2014 Schizophrenia Research Forum Privacy Policy Disclaimer Disclosure Copyright