ArticleComputational statistics & data analysis2009
The power of linkage analysis of a disease-related endophenotype using asymmetrically ascertained sib pairs.
Article in Computational statistics & data analysis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Thought Disorder in Schizophrenia and Bipolar Disorder Probands, Their Relatives, and Nonpsychiatric Controls.Schizophrenia bulletin · 2017Article
- Non-Mendelian etiologic factors in neuropsychiatric illness: pleiotropy, epigenetics, and convergence.The Behavioral and brain sciences · 2012Article
- Necessary and sufficient conditions for equality of sibling and parent-offspring risk of a disease endophenotype in case families.Annals of human genetics · 2012Article
- The Genetic Basis of Thought Disorder and Language and Communication Disturbances in Schizophrenia.Journal of neurolinguistics · 2010Article
- Tailoring the definition of the clinical schizophrenia phenotype in linkage studies.Schizophrenia research · 2010Article
- Family-based analysis of a myocardial infarction endophenotype: comparison of sampling designs.BMC proceedings · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
A linkage study of a qualitative disease endophenotype in a sample of sib pairs, consisting of one disease affected proband and one sibling is considered. The linkage statistic compares marker allele sharing with the proband in siblings with an abnormal endophenotype to siblings with the normal endophenotype. Expressions for the distribution of this linkage statistic, in terms of the recombination fraction are derived and (1) the genetic parameter values (allele frequency and endophenotype and disease penetrance) and (2) the abnormal endophenotype rates in the population and in classes of relatives of disease affected probands. It is then shown that when either the disease or the abnormal endophenotype has additive penetrance, the expressions simplify to a monotonic function of the difference between abnormal endophenotype rates in siblings and in the population. Thought disorder is considered as a putative schizophrenia endophenotype. Forty sets of genetic parameter values that correspond to the known prevalence values for thought disorder in schizophrenic patients, siblings of schizophrenics and the general population are evaluated. For these genetic parameter values, numerical results show that the test statistic has>70% power (α = 0.0001) in general with a sample of 200 or more proband-sibling pairs to detect the linkage between a marker (θ = 0.01), and a locus pleiotropic for schizophrenia and thought disorder.
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Registered trials
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