ArticleAmerican journal of human genetics2000
Linkage analysis in the presence of errors IV: joint pseudomarker analysis of linkage and/or linkage disequilibrium on a mixture of pedigrees and singletons when the mode of inheritance cannot be accurately specified.
Article in American journal of human genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed.
- Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea.The pharmacogenomics journal · 2007Trial
- A genome scan and follow-up study identify a bipolar disorder susceptibility locus on chromosome 1q42.Molecular psychiatry · 2004Trial
- Replication of 1q42 linkage in Finnish schizophrenia pedigrees.Molecular psychiatry · 2004Trial
- Neuregulin signaling pathway in smoking behavior.Translational psychiatry · 2017Article
- Article
- AMIGO-Kv2.1 Potassium Channel Complex Is Associated With Schizophrenia-Related Phenotypes.Schizophrenia bulletin · 2016Article
- Complex pedigrees in the sequencing era: to track transmissions or decorrelate?Genetic epidemiology · 2014Article
- Disease-related mutations among Caribbean Hispanics with familial dementia.Molecular genetics & genomic medicine · 2014Article
- Article
- PSEUDOMARKER 2.0: efficient computation of likelihoods using NOMAD.BMC bioinformatics · 2014Article
- Combined linkage and family-based association analysis improves candidate gene detection in Genetic Analysis Workshop 18 simulation data.BMC proceedings · 2014Article
- Role of nicotine dependence in the association between the dopamine receptor gene DRD3 and major depressive disorder.PloS one · 2014Article
- A large-scale candidate gene analysis of mood disorders: evidence of neurotrophic tyrosine kinase receptor and opioid receptor signaling dysfunction.Psychiatric genetics · 2013Article
- Analysis of detailed phenotype profiles reveals CHRNA5-CHRNA3-CHRNB4 gene cluster association with several nicotine dependence traits.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2012Article
- On the statistical properties of family-based association tests in datasets containing both pedigrees and unrelated case-control samples.European journal of human genetics : EJHG · 2012Article
- A potential novel spontaneous preterm birth gene, AR, identified by linkage and association analysis of X chromosomal markers.PloS one · 2012Article
- On the validity of the likelihood ratio test and consistency of resulting parameter estimates in joint linkage and linkage disequilibrium analysis under improperly specified parametric models.Annals of human genetics · 2012Article
- Family-based designs for genome-wide association studies.Nature reviews. Genetics · 2011Review
- Mapping a new spontaneous preterm birth susceptibility gene, IGF1R, using linkage, haplotype sharing, and association analysis.PLoS genetics · 2011Article
- Effective sample size: Quick estimation of the effect of related samples in genetic case-control association analyses.Computational biology and chemistry · 2011Article
9 more citing papers are in PubMed but not listed here.
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2 authors.
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Abstract
There is a lot of confusion in the literature about the "differences" between "model-based" and "model-free" methods and about which approach is better suited for detection of the genes predisposing to complex multifactorial phenotypes. By starting from first principles, we demonstrate that the differences between the two approaches have more to do with study design than statistical analysis. When simple data structures are repeatedly ascertained, no assumptions about the genotype-phenotype relationship need to be made for the analysis to be powerful, since simple data structures admit only a small number of df. When more complicated and/or heterogeneous data structures are ascertained, however, the number of df in the underlying probability model is too large to have a powerful, truly "model-free" test. So-called "model-free" methods typically simplify the underlying probability model by implicitly assuming that, in some sense, all meioses connecting two affected individuals are informative for linkage with identical probability and that the affected individuals in a pedigree share as many disease-predisposing alleles as possible. By contrast, "model-based" methods add structure to the underlying parameter space by making assumptions about the genotype-phenotype relationship, making it possible to probabilistically assign disease-locus genotypes to all individuals in the data set on the basis of the observed phenotypes. In this study, we demonstrate the equivalence of these two approaches in a variety of situations and exploit this equivalence to develop more powerful and efficient likelihood-based analogues of "model-free" tests of linkage and/or linkage disequilibrium. Through the use of a "pseudomarker" locus to structure the space of observations, sib-pairs, triads, and singletons can be analyzed jointly, which will lead to tests that are more well-behaved, efficient, and powerful than traditional "model-free" tests such as the affected sib-pair, transmission/disequilibrium, haplotype relative risk, and case-control tests. Also described is an extension of this approach to large pedigrees, which, in practice, is equivalent to affected relative-pair analysis. The proposed methods are equally applicable to two-point and multipoint analysis (using complex-valued recombination fractions).
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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.