GeneSet Information

Tier I GS270567 • GWAS Catalog Data for depressive episode measurement, bipolar disorder in 723 European ancestry cases

DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Depressive episodes in bipolar disorder. The EFO term depressive episode measurement, bipolar disorder was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: depressive episode measurement, bipolar disorder

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2019-01-07

SPECIES:

AUTHORS:

C Fabbri, A Serretti

TITLE:

Genetics of long-term treatment outcome in bipolar disorder.

JOURNAL:

Progress in neuro-psychopharmacology & biological psychiatry Feb 2016, Vol 65, pp. 17-24

ABSTRACT:

Bipolar disorder (BD) shows one of the strongest genetic predispositions among psychiatric disorders and the identification of reliable genetic predictors of treatment response could significantly improve the prognosis of the disease. The present study investigated genetic predictors of long-term treatment-outcome in 723 patients with BD type I from the STEP-BD (Systematic Treatment Enhancement Program for Bipolar Disorder) genome-wide dataset. BD I patients with >6months of follow-up and without any treatment restriction (reflecting a natural setting scenario) were included. Phenotypes were the total and depressive episode rates and the occurrence of one or more (hypo)manic/mixed episodes during follow-up. Quality control of genome-wide data was performed according to standard criteria and linear/logistic regression models were used as appropriate under an additive hypothesis. Top genes were further analyzed through a pathway analysis. Genes previously involved in the susceptibility to BD (DFNB31, SORCS2, NRXN1, CNTNAP2, GRIN2A, GRM4, GRIN2B), antidepressant action (DEPTOR, CHRNA7, NRXN1), and mood stabilizer or antipsychotic action (NTRK2, CHRNA7, NRXN1) may affect long-term treatment outcome of BD. Promising findings without previous strong evidence were TRAF3IP2-AS1, NFYC, RNLS, KCNJ2, RASGRF1, NTF3 genes. Pathway analysis supported particularly the involvement of molecules mediating the positive regulation of MAPK cascade and learning/memory processes. Further studies focused on the outlined genes may be helpful to provide validated markers of BD treatment outcome. PUBMED: 26297903
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