ReviewMolecular psychiatry2021
Translational genomics and beyond in bipolar disorder.
Review in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.
- Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology.Nature genetics · 2021Pooled it
- Genome-wide association study of early-onset bipolar I disorder in the Han Taiwanese population.Translational psychiatry · 2021Pooled it
- Explore the Mechanism of Xiaoyaosan for Treatment of Bipolar Disorder Based on Network Pharmacology, Experimental Validation and Molecular Docking.CNS neuroscience & therapeutics · 2026Article
- Bipolar disorder in an evolutionary framework: rethinking adaptation, vulnerability, and stigma.Frontiers in psychiatry · 2026Article
- Human mood disorder risk gene Synaptotagmin-14 contributes to mania-like behaviors in mice.Molecular psychiatry · 2025Article
- Psychiatric Genomics 2025: State of the Art and the Path Forward.The Psychiatric clinics of North America · 2025Review
- Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons.Nature communications · 2025Article
- Gain of bipolar disorder-related lncRNA AP1AR-DT in mice induces depressive and anxiety-like behaviors by reducing Negr1-mediated excitatory synaptic transmission.BMC medicine · 2024Article
- NEK4 modulates circadian fluctuations of emotional behaviors and synaptogenesis in male mice.Nature communications · 2024Article
- Review
- Processing speed mediates the relationship between DDR1 and psychosocial functioning in euthymic patients with bipolar disorder presenting psychotic symptoms.Molecular psychiatry · 2024Article
- ANK3 rs10994336 and ZNF804A rs7597593 polymorphisms: genetic interaction for emotional and behavioral symptoms of alcohol withdrawal syndrome.BMC psychiatry · 2024Article
- Screening, Genetic Variants, and Bipolar Disorders: Can Useful Hypotheses Arise from the Sum of Partial Failures?Clinics and practice · 2023Article
- Identification of a psychiatric risk gene NISCH at 3p21.1 GWAS locus mediating dendritic spine morphogenesis and cognitive function.BMC medicine · 2023Article
- Harnessing deep learning into hidden mutations of neurological disorders for therapeutic challenges.Archives of pharmacal research · 2023Review
- Bidirectional genetic overlap between bipolar disorder and intelligence.BMC medicine · 2022Article
- Pedigree-based study to identify GOLGB1 as a risk gene for bipolar disorder.Translational psychiatry · 2022Article
- dbBIP: a comprehensive bipolar disorder database for genetic research.Database : the journal of biological databases and curation · 2022Article
- Phenotypes, mechanisms and therapeutics: insights from bipolar disorder GWAS findings.Molecular psychiatry · 2022Review
- Functional genomic analysis delineates regulatory mechanisms of GWAS-identified bipolar disorder risk variants.Genome medicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) have revealed multiple genomic loci conferring risk of bipolar disorder (BD), providing hints for its underlying pathobiology. However, there are still remaining questions to answer. For example, discordance exists between BD heritability estimated with earlier epidemiological evidence and that calculated based on common GWAS variations. Where is the "missing heritability"? How can we explain the biology of the disease based on genetic findings? In this review, we summarize the accomplishments and limitations of current BD GWAS, and discuss potential reasons for the "missing heritability." In addition, progresses of research for the biological mechanisms underlying BD genetic risk using brain tissues, reprogrammed cells, and model animals are reviewed. While our knowledge of BD genetic basis is significantly promoted by these efforts, the complexities of gene regulation in the genome, the spatial-temporal heterogeneity during brain development, and the limitations of different experimental models should always be considered. Notably, several genes have been widely studied given their relatively well-characterized involvement in BD (e.g., CACAN1C and ANK3), and findings of these genes are summarized to both outline possible biological mechanisms of BD and describe examples of translating GWAS discoveries into the pathophysiology.
Indexed as
Identifiers
What OpenQuestion holds
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.