ArticleMolecular psychiatry2012
Genome-wide survey implicates the influence of copy number variants (CNVs) in the development of early-onset bipolar disorder.
Article in Molecular psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 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
- Higher frequencies of CNV deletions in bipolar disorder among Chinese Population.Molecular psychiatry · 2026Article
- Contribution of copy number variations to education, socioeconomic status and cognition from a genome-wide study of 305,401 subjects.Molecular psychiatry · 2025Article
- Article
- Copy Number Variations in Neuropsychiatric Disorders.International journal of molecular sciences · 2023Review
- The contribution of copy number variants to psychiatric symptoms and cognitive ability.Molecular psychiatry · 2023Review
- Psychosocial markers of age at onset in bipolar disorder: a machine learning approach.BJPsych open · 2022Article
- dbBIP: a comprehensive bipolar disorder database for genetic research.Database : the journal of biological databases and curation · 2022Article
- Bipolar disorder: Trimodal age-at-onset distribution.Bipolar disorders · 2021Review
- Genetic Pathways and Functional Subnetworks for the Complex Nature of Bipolar Disorder in Genome-Wide Association Study.Frontiers in molecular neuroscience · 2021Article
- The Co-existence of ADHD With Autism in Saudi Children: An Analysis Using Next-Generation DNA Sequencing.Frontiers in genetics · 2020Article
- Contribution of Rare Copy Number Variants to Bipolar Disorder Risk Is Limited to Schizoaffective Cases.Biological psychiatry · 2019Article
- [Breakthrough in understanding the molecular causes of psychiatric disorders].Der Nervenarzt · 2019Review
- Identification of potential genetic risk factors for bipolar disorder by whole-exome sequencing.Translational psychiatry · 2018Article
- An examination of multiple classes of rare variants in extended families with bipolar disorder.Translational psychiatry · 2018Article
- Schizophrenia and the neurodevelopmental continuum:evidence from genomics.World psychiatry : official journal of the World Psychiatric Association (WPA) · 2017Article
- Genomic Disorders in Psychiatry-What Does the Clinician Need to Know?Current psychiatry reports · 2017Review
- [Genetics of bipolar disorder].Der Nervenarzt · 2017Review
- Stability and change in reported age of onset of depression, back pain, and smoking over 29 years in a prospective cohort study.Journal of psychiatric research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
We used genome-wide single nucleotide polymorphism (SNP) data to search for the presence of copy number variants (CNVs) in 882 patients with bipolar disorder (BD) and 872 population-based controls. A total of 291 (33%) patients had an early age-at-onset < or =21 years (AO < or =21 years). We systematically filtered for CNVs that cover at least 30 consecutive SNPs and which directly affect at least one RefSeq gene. We tested whether (a) the genome-wide burden of these filtered CNVs differed between patients and controls and whether (b) the frequency of specific CNVs differed between patients and controls. Genome-wide burden analyses revealed that the frequency and size of CNVs did not differ substantially between the total samples of BD patients and controls. However, separate analysis of patients with AO < or =21 years and AO>21 years showed that the frequency of microduplications was significantly higher (P=0.0004) and the average size of singleton microdeletions was significantly larger (P=0.0056) in patients with AO < or =21 years compared with controls. A search for specific BD-associated CNVs identified two common CNVs: (a) a 160 kb microduplication on 10q11 was overrepresented in AO < or = 21 years patients (9.62%) compared with controls (3.67%, P=0.0005) and (b) a 248 kb microduplication on 6q27 was overrepresented in the AO< or = 21 years subgroup (5.84%) compared with controls (2.52%, P=0.0039). These data suggest that CNVs have an influence on the development of early-onset, but not later-onset BD. Our study provides further support for previous hypotheses of an etiological difference between early-onset and later-onset BD.
Indexed as
Identifiers
21358712What 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.