ArticleMolecular psychiatry2000
Family-based linkage disequilibrium mapping using SNP marker haplotypes: application to a potential locus for schizophrenia at chromosome 22q11.
Article in Molecular psychiatry, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- The impact of COMT, BDNF and 5-HTT brain-genes on the development of anorexia nervosa: a systematic review.Eating and weight disorders : EWD · 2021Pooled it
- Separate and interacting effects within the catechol-O-methyltransferase (COMT) are associated with schizophrenia.Molecular psychiatry · 2005Trial
- Haplotypic association spanning the 22q11.21 genes COMT and ARVCF with schizophrenia.Molecular psychiatry · 2005Trial
- A Genetic Evaluation System for New Zealand White Rabbit Germplasm Resources Based on SSR Markers.Animals : an open access journal from MDPI · 2020Article
- Neuroimaging genomics in psychiatry-a translational approach.Genome medicine · 2017Review
- Linkage and Association Analyses of Schizophrenia with Genetic Variations on Chromosome 22q11 in Koreans.Psychiatry investigation · 2016Article
- Morphological changes in gray matter volume correlate with catechol-O-methyl transferase gene Val158Met polymorphism in first-episode treatment-naïve patients with schizophrenia.Neuroscience bulletin · 2015Article
- Biological effects of COMT haplotypes and psychosis risk in 22q11.2 deletion syndrome.Biological psychiatry · 2014Article
- Article
- A functional variant provided further evidence for the association of ARVCF with schizophrenia.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2010Article
- The complex global pattern of genetic variation and linkage disequilibrium at catechol-O-methyltransferase.Molecular psychiatry · 2010Article
- A network of dopaminergic gene variations implicated as risk factors for schizophrenia.Human molecular genetics · 2008Article
- Genetic variation in catechol-O-methyltransferase: effects on working memory in schizophrenic patients, their siblings, and healthy controls.Biological psychiatry · 2008Article
- Dopamine genes and schizophrenia: case closed or evidence pending?Schizophrenia bulletin · 2007Review
- Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression.Molecular psychiatry · 2007Article
- Is COMT a susceptibility gene for schizophrenia?Schizophrenia bulletin · 2007Review
- Evidence for statistical epistasis between catechol-O-methyltransferase (COMT) and polymorphisms in RGS4, G72 (DAOA), GRM3, and DISC1: influence on risk of schizophrenia.Human genetics · 2007Article
- Treatment of cognitive deficits associated with schizophrenia: potential role of catechol-O-methyltransferase inhibitors.CNS drugs · 2007Review
- The catechol-O-methyl transferase (COMT) gene as a candidate for psychiatric phenotypes: evidence and lessons.Molecular psychiatry · 2006Review
- The quantification of COMT mRNA in post mortem cerebellum tissue: diagnosis, genotype, methylation and expression.BMC medical genetics · 2006Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Family-based linkage disequilibrium mapping using SNP markers is expected to be a major route to the identification of susceptibility alleles for complex diseases. However there are a number of methodological issues yet to be resolved, including the handling of extended haplotype data and analysis of haplotype transmission in sib-pair or family trio samples. In the present study, we have analysed two dinucleotide repeat and six SNP markers at the COMT locus at chromosome 22q11, a region implicated in psychosis, for transmission distortion in 198 Chinese schizophrenic family trios. When individual markers were analysed using the TDT, two showed modest evidence of transmission distortion (186C/T, P = 0.04; Val158Met, P = 0.01). Using haplotypes of paired markers analysed by the program TRANSMIT, the most significant P value was 0.001, for the Met158Val and 900ins/delC polymorphisms in the COMT gene. The global P value for the haplotypes of all six SNP markers tested was 0.004, largely a result of the excess transmission of two extended haplotypes which differed at the marker 408C/G. The exclusion of this marker from the analysis gave a global P value of 0.002 and produced a five marker haplotype system which was significant at P = 0.0006. This haplotype consisted of the alleles -287G:186C:Val158:900insC:ARVCF930C, which may represent a background haplotype for the transmission of a schizophrenia susceptibility allele at chromosome 22q11. Our results support the hypotheses that either COMT is itself a susceptibility gene, or more likely that this region of chromosome 22 contains a susceptibility gene that is in linkage disequilibrium with COMT alleles. Molecular Psychiatry (2000) 5, 77-84.
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