ArticleAmerican journal of human genetics1995
Mathematical limits of multilocus models: the genetic transmission of bipolar disorder.
Article in American journal of human genetics, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.
- Systematic review of genome-wide gene expression studies of bipolar disorder.BMC psychiatry · 2013Pooled it
- Genome scan meta-analysis of schizophrenia and bipolar disorder, part III: Bipolar disorder.American journal of human genetics · 2003Pooled it
- Polygenic risk score for bipolar disorder associates with divergent thinking and brain structures in the prefrontal cortex.Human brain mapping · 2021Article
- Pathway-induced allelic spectra of diseases in the presence of strong genetic effects.Human genetics · 2018Article
- Rare deleterious mutations are associated with disease in bipolar disorder families.Molecular psychiatry · 2017Article
- Toward a Deeper Understanding of the Genetics of Bipolar Disorder.Frontiers in psychiatry · 2015Review
- Analysis of ANK3 and CACNA1C variants identified in bipolar disorder whole genome sequence data.Bipolar disorders · 2014Article
- Genetic relationships between schizophrenia, bipolar disorder, and schizoaffective disorder.Schizophrenia bulletin · 2014Review
- Gene expression alterations in bipolar disorder postmortem brains.Bipolar disorders · 2013Article
- Sporadic cases are the norm for complex disease.European journal of human genetics : EJHG · 2010Article
- The genetic interpretation of area under the ROC curve in genomic profiling.PLoS genetics · 2010Article
- Multi-locus models of genetic risk of disease.Genome medicine · 2010Article
- Association study of 21 circadian genes with bipolar I disorder, schizoaffective disorder, and schizophrenia.Bipolar disorders · 2009Article
- Genome-wide association study of bipolar disorder in European American and African American individuals.Molecular psychiatry · 2009Article
- Genetics of psychosis; insights from views across the genome.Human genetics · 2009Review
- Psychosis genetics: modeling the relationship between schizophrenia, bipolar disorder, and mixed (or "schizoaffective") psychoses.Schizophrenia bulletin · 2009Article
- Gene-wide analyses of genome-wide association data sets: evidence for multiple common risk alleles for schizophrenia and bipolar disorder and for overlap in genetic risk.Molecular psychiatry · 2009Article
- Association analysis of monoamine oxidase A gene and bipolar affective disorder in Han Chinese.Behavioral and brain functions : BBF · 2008Article
- Genetics of bipolar disorder.Dialogues in clinical neuroscience · 2008Review
- Association analysis of the chromosome 4p-located G protein-coupled receptor 78 (GPR78) gene in bipolar affective disorder and schizophrenia.Molecular psychiatry · 2006Article
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 1 institution in 1 country.
Funding
Abstract
We describe a simple, graphical method for determining plausible modes of inheritance for complex traits and apply this to bipolar disorder. The constraints that allele frequencies and penetrances lie in the interval 0-1 impose limits on recurrence risks, KR, in relatives of an affected proband for a given population prevalence, KP. We have investigated these limits for KR in three classes of relatives (MZ co-twin, sibling, and parent/offspring) for the general single-locus model and for two types of multilocus models: heterogeneity and multiplicative. In our models we have assumed Hardy-Weinberg equilibrium, an all-or-none trait, absence of nongenetic resemblance between relatives, and negligible mutation at the disease loci. Although the true values of KP and the KR's are only approximately known, observed population and family data for bipolar disorder are inconsistent with a single-locus model or with any heterogeneity model. In contrast, multiplicative models involving three or more loci are consistent with observed data and, thus, represent plausible models for the inheritance of bipolar disorders. Studies to determine the genetic basis of most bipolar disorder should use methods capable of detecting interacting oligogenes.
Indexed as
Identifiers
7668299PMC1801283W1764932013What 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.