The involvement of GSK3β in bipolar disorder: Integrating evidence from multiple types of genetic studies

@article{Luykx2010TheIO,
  title={The involvement of GSK3$\beta$ in bipolar disorder: Integrating evidence from multiple types of genetic studies},
  author={Jurjen J. Luykx and Marco P. M. Boks and A.P.R. Terwindt and Steven C. Bakker and R. S. Kahn and Roel A. Ophoff},
  journal={European Neuropsychopharmacology},
  year={2010},
  volume={20},
  pages={357-368}
}

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References

SHOWING 1-10 OF 117 REFERENCES
Rapid Publication Increase in GSK 3 b Gene Copy Number Variation in Bipolar Disorder
TLDR
The finding that patients with BD have an increased frequency of this CNV suggests that GSK3b may be involved in BD susceptibility in some individuals and that CNVs in this and other candidate genes for psychiatric disorders should be analyzed as causative functional genetic variants.
The genetics of bipolar disorder: genome ‘hot regions,’ genes, new potential candidates and future directions
TLDR
The combination of linkage and association approaches provided a number of liability genes in BP, Nevertheless, other approaches are required to disentangle conflicting findings, such as gene interaction analyses, interaction with psychosocial and environmental factors and, finally, endophenotype investigations.
Association study of Wnt signaling pathway genes in bipolar disorder.
TLDR
Evidence for association of bipolar disorder with PPARD, a gene in the Wnt signaling pathway is found, a new avenue for understanding the pathogenesis of severe bipolar disorder and developing more effective treatments.
Convergent functional genomics of genome‐wide association data for bipolar disorder: Comprehensive identification of candidate genes, pathways and mechanisms
  • H. Le-Niculescu, S. Patel, A. Niculescu
  • Biology
    American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics
  • 2009
TLDR
This analysis is the most comprehensive integration of genetics and functional genomics to date in the field of bipolar disorder, yielding a series of novel candidate genes, blood biomarkers, as well as a comprehensive identification of pathways and mechanisms.
Lithium response and genetic variation in the CREB family of genes
TLDR
Results suggest that the CREB1‐1H SNP (G/A change, P < 0.002) and the CREb1‐7H SNP may be associated with BD and/or lithium response and classification according to Li response is a manner through which more homogeneous populations can be obtained for investigation.
Combined analysis from eleven linkage studies of bipolar disorder provides strong evidence of susceptibility loci on chromosomes 6q and 8q.
TLDR
It is demonstrated that combining original genome-scan data is a powerful approach for the elucidation of linkage regions underlying complex disease, and genomewide significant linkage to BP on chromosomes 6q and 8q is established.
Whole-genome association study of bipolar disorder
TLDR
A comparison of the strongest associations with the genome-wide scan of 1868 patients with BP disorder and 2938 controls who completed the scan as part of the Wellcome Trust Case–Control Consortium indicates concordant signals for SNPs within the voltage-dependent calcium channel, L-type, alpha 1C subunit (CACNA1C) gene.
A genome-wide association study implicates diacylglycerol kinase eta (DGKH) and several other genes in the etiology of bipolar disorder
TLDR
This first genome-wide association study of bipolar disorder shows that several genes, each of modest effect, reproducibly influence disease risk and may be a polygenic disease.
Candidate genes, pathways and mechanisms for bipolar (manic–depressive) and related disorders: an expanded convergent functional genomics approach
TLDR
Data from a relevant pharmacogenomic mouse model and human data combined with human data suggest that more primitive molecular mechanisms involved in pleasure and pain may have been recruited by evolution to play a role in higher mental functions such as mood.
Stargazin involvement with bipolar disorder and response to lithium treatment
TLDR
Stargazin dysregulation may be involved with the pathophysiology of BPD, but not with that of schizophrenia, and that Stargazin polymorphisms may play a role in the response to lithium treatment.
...
1
2
3
4
5
...