ArticleShanghai archives of psychiatry2015
Gene-based and pathway-based genome-wide association study of alcohol dependence.
Article in Shanghai archives of psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- A data driven approach to identify trajectories of prenatal alcohol consumption in an Australian population-based cohort of pregnant women.Scientific reports · 2022Article
- Model-based assessment of replicability for genome-wide association meta-analysis.Nature communications · 2021Article
- Review
- Hippocampal transcriptome reveals novel targets of FASD pathogenesis.Brain and behavior · 2019Article
- Shared additive genetic variation for alcohol dependence among subjects of African and European ancestry.Addiction biology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe organization of risk genes within signaling pathways may provide clues about the converging neurobiological effects of risk genes for alcohol dependence.
aimIdentify risk genes and risk gene pathways for alcohol dependence.
methodsWe conducted a pathway-based genome-wide association study (GWAS) of alcohol dependence using a gene-set-rich analytic approach. Approximately one million genetic markers were tested in the discovery sample which included 1409 European-American (EA) alcohol dependent individuals and 1518 EA healthy comparison subjects. An additional 681 African-American (AA) cases and 508 AA healthy subjects served as the replication sample.
resultsWe identified several genome-wide replicable risk genes and risk pathways that were significantly associated with alcohol dependence. After applying the Bonferroni correction for multiple testing, the 'cellextracellular matrix interactions' pathway (p<2.0E-4 in EAs) and the PXN gene (which encodes paxillin) (p=3.9E-7 in EAs) within this pathway were the most promising risk factors for alcohol dependence. There were also two nominally replicable pathways enriched in alcohol dependence-related genes in both EAs (0.015≤p≤0.035) and AAs (0.025≤p≤0.050): the 'Na+/Cl- dependent neurotransmitter transporters' pathway and the 'other glycan degradation' pathway.
conclusionThese findings provide new evidence highlighting several genes and biological signaling processes that may be related to the risk for alcohol dependence.
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