ArticlePsychiatric genetics2008
Posterior probability of linkage analysis of autism dataset identifies linkage to chromosome 16.
Article in Psychiatric genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed, 11 citations in OpenAlex.
- An increase in Semaphorin 3A biases the axonal direction and induces an aberrant dendritic arborization in an in vitro model of human neural progenitor differentiation.Cell & bioscience · 2022Article
- Association between C-Maf-inducing protein gene rs2287112 polymorphism and schizophrenia.PeerJ · 2021Article
- High-resolution chromosomal microarray analysis for copy-number variations in high-functioning autism reveals large aberration typical for intellectual disability.Journal of neural transmission (Vienna, Austria : 1996) · 2020Article
- Gene expression profiling differentiates autism case-controls and phenotypic variants of autism spectrum disorders: evidence for circadian rhythm dysfunction in severe autism.Autism research : official journal of the International Society for Autism Research · 2009Article
- Genetic testing in children with autism spectrum disorders.Anadolu psikiyatri dergisiArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveTo apply phenotypic and statistical methods designed to account for heterogeneity to linkage analyses of the autism Collaborative Linkage Study of Autism (CLSA) affected sibling pair families.
methodThe CLSA contains two sets of 57 families each; Set 1 has been analyzed previously, whereas this study presents the first analyses of Set 2. The two sets were analyzed independently, and were further split based on the degree of phrase speech delay in the siblings. Linkage analysis was carried out using the posterior probability of linkage (PPL), a Bayesian statistic that provides a mathematically rigorous mechanism for combining linkage evidence across multiple samples.
resultsTwo-point PPLs from Set 1 led to the follow-up genotyping of 18 markers around linkage peaks on 1q, 13p, 13q, 16q, and 17q in both sets of families. Multipoint PPLs were then calculated for the entire CLSA sample. These analyses identified four regions with at least modest evidence in support of linkage: 1q at 173 cM, PPL=0.12; 13p at 21 cM, PPL=0.16; 16q at 63 cM, PPL=0.36; Xq at 40 cM, PPL=0.11.
conclusionWe find strengthened evidence for linkage of autism to chromosomes 1q, 13p, 16q, and Xq, and diminished evidence for linkage to 7q and 13q. The verity of these findings will be tested by continuing to update our PPL analyses with data from additional autism datasets.
Indexed as
Identifiers
What 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.