ArticleProceedings of the National Academy of Sciences of the United States of America2015
Rare variants in neuronal excitability genes influence risk for bipolar disorder.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 8 of them syntheses that pooled it.
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Who cites it
101 citing papers in PubMed, 8 syntheses or guidelines pooled it, 183 citations in OpenAlex.
- Neurophysiological profiles of patients with bipolar disorders as probed with transcranial magnetic stimulation: A systematic review.Neuropsychopharmacology reports · 2024Pooled it
- Structural connectivity associated with familial risk for mental illness: A meta-analysis of diffusion tensor imaging studies in relatives of patients with severe mental disorders.Human brain mapping · 2022Pooled it
- Investigating rare pathogenic/likely pathogenic exonic variation in bipolar disorder.Molecular psychiatry · 2021Pooled it
- The genetic overlap between mood disorders and cardiometabolic diseases: a systematic review of genome wide and candidate gene studies.Translational psychiatry · 2017Pooled it
- A systematic review of calcium channel antagonists in bipolar disorder and some considerations for their future development.Molecular psychiatry · 2016Pooled it
- Exome Sequencing of Familial Bipolar Disorder.JAMA psychiatry · 2016Pooled it
- Pooled it
- Addiction pharmacogenetics: a systematic review of the genetic variation of the dopaminergic system.Psychiatric genetics · 2015Pooled it
- Explore the Mechanism of Xiaoyaosan for Treatment of Bipolar Disorder Based on Network Pharmacology, Experimental Validation and Molecular Docking.CNS neuroscience & therapeutics · 2026Article
- Therapeutic Overlap Between Bipolar Disorder and Migraine: A Systematic Review of Pharmacological Trials.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Genetic and neuroanatomical correlates of bipolar disorder in high-risk youth.BMJ mental health · 2026Article
- Deletion of the Voltage-Gated Calcium Channel Gene, CaCerebellum (London, England) · 2025Article
- Remote spatial memory deficits in mouse models of neuropsychiatric disorders with immature dentate gyrus phenotype.The international journal of neuropsychopharmacology · 2025Article
- Stress-induced altered expression of hippocampal nuclear and mitochondrial encoded genes in rats and cross-species genetic associations reveal molecular links to depression.The international journal of neuropsychopharmacology · 2025Article
- The Impact of Overexpression of the Mouse Ortholog ofBiological psychiatry global open science · 2025Article
- Proteostasis regulation of GABABiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Inhibition of NMDA receptors and other ion channel types by membrane-associated drugs.Frontiers in pharmacology · 2025Review
- A genetically encoded actuator boosts L-type calcium channel function in diverse physiological settings.Science advances · 2024Article
- The L-type calcium channel CaV1.3: A potential target for cancer therapy.Journal of cellular and molecular medicine · 2024Review
- Altered neuroepithelial morphogenesis and migration defects in iPSC-derived cerebral organoids and 2D neural stem cells in familial bipolar disorder.Oxford open neuroscience · 2024Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
25 authors at 9 institutions in 2 countries.
Funding
Abstract
We sequenced the genomes of 200 individuals from 41 families multiply affected with bipolar disorder (BD) to identify contributions of rare variants to genetic risk. We initially focused on 3,087 candidate genes with known synaptic functions or prior evidence from genome-wide association studies. BD pedigrees had an increased burden of rare variants in genes encoding neuronal ion channels, including subunits of GABAA receptors and voltage-gated calcium channels. Four uncommon coding and regulatory variants also showed significant association, including a missense variant in GABRA6. Targeted sequencing of 26 of these candidate genes in an additional 3,014 cases and 1,717 controls confirmed rare variant associations in ANK3, CACNA1B, CACNA1C, CACNA1D, CACNG2, CAMK2A, and NGF. Variants in promoters and 5' and 3' UTRs contributed more strongly than coding variants to risk for BD, both in pedigrees and in the case-control cohort. The genes and pathways identified in this study regulate diverse aspects of neuronal excitability. We conclude that rare variants in neuronal excitability genes contribute to risk for BD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.