ArticleMolecular psychiatry2007
Genome-wide linkage scan of 98 bipolar pedigrees and analysis of clinical covariates.
Article in Molecular psychiatry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The genetics of early-onset bipolar disorder: A systematic review.Journal of affective disorders · 2015Pooled it
- Pooled it
- Association between the Arylalkylamine N-Acetyltransferase (AANAT) Gene and Seasonality in Patients with Bipolar Disorder.Psychiatry investigation · 2021Article
- The null distribution of likelihood-ratio statistics in the conditional-logistic linkage model.Frontiers in genetics · 2013Article
- Genome-wide significant association between a 'negative mood delusions' dimension in bipolar disorder and genetic variation on chromosome 3q26.1.Translational psychiatry · 2012Article
- Genome-wide linkage analysis of 972 bipolar pedigrees using single-nucleotide polymorphisms.Molecular psychiatry · 2012Article
- Article
- Association study of serotonin pathway genes in attempted suicide.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2012Article
- Convergent functional genomic studies of ω-3 fatty acids in stress reactivity, bipolar disorder and alcoholism.Translational psychiatry · 2011Article
- Genome-wide association analysis of age at onset and psychotic symptoms in bipolar disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2011Article
- Article
- Case-control association study of TGOLN2 in attempted suicide.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2010Article
- A genome-wide linkage study of bipolar disorder and co-morbid migraine: replication of migraine linkage on chromosome 4q24, and suggestion of an overlapping susceptibility region for both disorders on chromosome 20p11.Journal of affective disorders · 2010Article
- Sex differences in TTC12/ANKK1 haplotype associations with daily tobacco smoking in Black and White Americans.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2010Article
- Article
- The genetics of bipolar disorder: genome 'hot regions,' genes, new potential candidates and future directions.Molecular psychiatry · 2008Review
- Current research in child and adolescent bipolar disorder.Dialogues in clinical neuroscience · 2008Review
- Genetics of bipolar disorder.Dialogues in clinical neuroscience · 2008Review
- Genetics of bipolar disorder.Current psychiatry reports · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Despite compelling evidence that genetic factors contribute to bipolar disorder (BP), attempts to identify susceptibility genes have met with limited success. This may be due to the genetic heterogeneity of the disorder. We sought to identify susceptibility loci for BP in a genome-wide linkage scan with and without clinical covariates that might reflect the underlying heterogeneity of the disorder. We genotyped 428 subjects in 98 BP families at the Center for Inherited Disease Research with 402 microsatellite markers. We first carried out a non-parametric linkage analysis with MERLIN, and then reanalyzed the data with LODPAL to incorporate clinical covariates for age at onset (AAO), psychosis and comorbid anxiety. We sought to further examine the top findings in the covariate analysis in an independent sample of 64 previously collected BP families. In the non-parametric linkage analysis, three loci were nominally significant under a narrow diagnostic model and seven other loci were nominally significant under a broader model. The top findings were on chromosomes 2q24 and 3q28. The covariate analyses yielded additional evidence for linkage on 3q28 with AAO in the primary and independent samples. Although none of the linked loci were genome-wide significant, their congruence with prior results and, for the covariate analyses, their identification in two separate samples increases the likelihood that they are true positives and deserve further investigation. These findings further demonstrate the value of considering clinical features that may reflect the underlying heterogeneity of disease in order to facilitate gene mapping.
Indexed as
Identifiers
17505464What 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.