ArticlePloS one2014
Common and rare variant analysis in early-onset bipolar disorder vulnerability.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Genome-wide association study of early-onset bipolar I disorder in the Han Taiwanese population.Translational psychiatry · 2021Pooled it
- The genetics of early-onset bipolar disorder: A systematic review.Journal of affective disorders · 2015Pooled it
- Cryptic mutations of PLC family members in brain disorders: recent discoveries and a deep-learning-based approach.Brain : a journal of neurology · 2023Review
- CADPS functional mutations in patients with bipolar disorder increase the sensitivity to stress.Molecular psychiatry · 2022Article
- Characterisation of age and polarity at onset in bipolar disorder.The British journal of psychiatry : the journal of mental science · 2021Article
- PLEKHA5, PLEKHA6, and PLEKHA7 bind to PDZD11 to target the Menkes ATPase ATP7A to the cell periphery and regulate copper homeostasis.Molecular biology of the cell · 2021Article
- WW, PH and C-Terminal Domains Cooperate to Direct the Subcellular Localizations of PLEKHA5, PLEKHA6 and PLEKHA7.Frontiers in cell and developmental biology · 2021Article
- Genetic Variants of theGenes · 2020Article
- Contribution of common and rare damaging variants in familial forms of bipolar disorder and phenotypic outcome.Translational psychiatry · 2020Article
- Investigating polygenic burden in age at disease onset in bipolar disorder: Findings from an international multicentric study.Bipolar disorders · 2019Article
- Reduced Expression ofFrontiers in endocrinology · 2019Article
- Identification of potential genetic risk factors for bipolar disorder by whole-exome sequencing.Translational psychiatry · 2018Article
- Clinical correlates of age at onset distribution in bipolar disorder: a comparison between diagnostic subgroups.International journal of bipolar disorders · 2017Article
- Correlation profiling of brain sub-cellular proteomes reveals co-assembly of synaptic proteins and subcellular distribution.Scientific reports · 2017Article
- Interaction between SLC6A4 promoter variants and childhood trauma on the age at onset of bipolar disorders.Scientific reports · 2015Article
- Association of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism with early-onset bipolar disorder.Bipolar disorders · 2015Article
- Genetic association study of circadian genes with seasonal pattern in bipolar disorders.Scientific reports · 2015Article
- Genetic Risk Score Analysis in Early-Onset Bipolar Disorder.The Journal of clinical psychiatryArticle
Corrections and comments
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Authors and funding
32 authors.
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Abstract
Bipolar disorder is one of the most common and devastating psychiatric disorders whose mechanisms remain largely unknown. Despite a strong genetic contribution demonstrated by twin and adoption studies, a polygenic background influences this multifactorial and heterogeneous psychiatric disorder. To identify susceptibility genes on a severe and more familial sub-form of the disease, we conducted a genome-wide association study focused on 211 patients of French origin with an early age at onset and 1,719 controls, and then replicated our data on a German sample of 159 patients with early-onset bipolar disorder and 998 controls. Replication study and subsequent meta-analysis revealed two genes encoding proteins involved in phosphoinositide signalling pathway (PLEKHA5 and PLCXD3). We performed additional replication studies in two datasets from the WTCCC (764 patients and 2,938 controls) and the GAIN-TGen cohorts (1,524 patients and 1,436 controls) and found nominal P-values both in the PLCXD3 and PLEKHA5 loci with the WTCCC sample. In addition, we identified in the French cohort one affected individual with a deletion at the PLCXD3 locus and another one carrying a missense variation in PLCXD3 (p.R93H), both supporting a role of the phosphatidylinositol pathway in early-onset bipolar disorder vulnerability. Although the current nominally significant findings should be interpreted with caution and need replication in independent cohorts, this study supports the strategy to combine genetic approaches to determine the molecular mechanisms underlying bipolar disorder.
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