ArticlePloS one2012
A fine-mapping study of 7 top scoring genes from a GWAS for major depressive disorder.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.
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Who cites it
20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.
- Genetic Landscape of Major Depressive Disorder: Assessment of Potential Diagnostic and Antidepressant Response Markers.The international journal of neuropsychopharmacology · 2023Pooled it
- Genome-wide pathway analysis in major depressive disorder.Journal of molecular neuroscience : MN · 2013Pooled it
- Deletion of Fgf14 confers resilience to basal and stress-induced depressive-like behavior and reduces anxiety in mice.Translational psychiatry · 2025Article
- Advances and Challenges in Depression Marker Research.Neuropsychiatric disease and treatment · 2025Review
- NaJournal of neural transmission (Vienna, Austria : 1996) · 2021Review
- Analysis of Major Depression Risk Genes Reveals Evolutionary Conservation, Shared Phenotypes, and Extensive Genetic Interactions.Frontiers in psychiatry · 2021Article
- Emerging roles of Fgf14 in behavioral control.Behavioural brain research · 2019Article
- Functional Modulation of Voltage-Gated Sodium Channels by a FGF14-Based Peptidomimetic.ACS chemical neuroscience · 2018Article
- Comparative Analysis of Gene Expression Profiles Involved in Calcium Signaling Pathways Using the NLVH Animal Model of Schizophrenia.Journal of molecular neuroscience : MN · 2018Article
- PPARgamma agonists rescue increased phosphorylation of FGF14 at S226 in the Tg2576 mouse model of Alzheimer's disease.Experimental neurology · 2017Article
- Intracellular Fibroblast Growth Factor 14: Emerging Risk Factor for Brain Disorders.Frontiers in cellular neuroscience · 2017Review
- CK2 activity is required for the interaction of FGF14 with voltage-gated sodium channels and neuronal excitability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Identification of Amino Acid Residues in Fibroblast Growth Factor 14 (FGF14) Required for Structure-Function Interactions with Voltage-gated Sodium Channel Nav1.6.The Journal of biological chemistry · 2016Article
- Genetic deletion of fibroblast growth factor 14 recapitulates phenotypic alterations underlying cognitive impairment associated with schizophrenia.Translational psychiatry · 2016Article
- Identifying a kinase network regulating FGF14:Nav1.6 complex assembly using split-luciferase complementation.PloS one · 2015Article
- Role of the axonal initial segment in psychiatric disorders: function, dysfunction, and intervention.Frontiers in psychiatry · 2014Review
- Modulation of the FGF14:FGF14 homodimer interaction through short peptide fragments.CNS & neurological disorders drug targets · 2014Article
- Reconceptualizing major depressive disorder as an infectious disease.Biology of mood & anxiety disorders · 2014Article
- Epistatic effects on abdominal fat content in chickens: results from a genome-wide SNP-SNP interaction analysis.PloS one · 2013Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Major depressive disorder (MDD) is a psychiatric disorder that is characterized--amongst others--by persistent depressed mood, loss of interest and pleasure and psychomotor retardation. Environmental circumstances have proven to influence the aetiology of the disease, but MDD also has an estimated 40% heritability, probably with a polygenic background. In 2009, a genome wide association study (GWAS) was performed on the Dutch GAIN-MDD cohort. A non-synonymous coding single nucleotide polymorphism (SNP) rs2522833 in the PCLO gene became only nominally significant after post-hoc analysis with an Australian cohort which used similar ascertainment. The absence of genome-wide significance may be caused by low SNP coverage of genes. To increase SNP coverage to 100% for common variants (m.a.f.>0.1, r(2)>0.8), we selected seven genes from the GAIN-MDD GWAS: PCLO, GZMK, ANPEP, AFAP1L1, ST3GAL6, FGF14 and PTK2B. We genotyped 349 SNPs and obtained the lowest P-value for rs2715147 in PCLO at P = 6.8E-7. We imputed, filling in missing genotypes, after which rs2715147 and rs2715148 showed the lowest P-value at P = 1.2E-6. When we created a haplotype of these SNPs together with the non-synonymous coding SNP rs2522833, the P-value decreased to P = 9.9E-7 but was not genome wide significant. Although our study did not identify a more strongly associated variant, the results for PCLO suggest that the causal variant is in high LD with rs2715147, rs2715148 and rs2522833.
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Registered trials
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