ArticleAmerican journal of human genetics2001
Maternal folate polymorphisms and the etiology of human nondisjunction.
Article in American journal of human genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 79 citations in OpenAlex.
- Fission Yeast Methylenetetrahydrofolate Reductase Ensures Mitotic and Meiotic Chromosome Segregation Fidelity.International journal of molecular sciences · 2021Article
- Polymorphisms in the MTHFR gene influence embryo viability and the incidence of aneuploidy.Human genetics · 2016Article
- Methylenetetrahydrofolate reductase polymorphism is not risk factor for Down syndrome in North India.Indian journal of human genetics · 2014Article
- The trisomy 18 syndrome.Orphanet journal of rare diseases · 2012Review
- Article
- Homocysteine and related genetic polymorphisms in Down's syndrome IQ.Journal of neurology, neurosurgery, and psychiatry · 2005Article
- Is there a familial link between Down's syndrome and neural tube defects? Population and familial survey.BMJ (Clinical research ed.) · 2004Article
- The origin of abnormalities in recurrent aneuploidy/polyploidy.American journal of human genetics · 2001Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Attempts to identify genetic contributors to human meiotic nondisjunction have met with little, if any, success. Thus, recent reports linking Down syndrome to maternal polymorphisms at either of two folate metabolism enzymes, methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR), have generated considerable interest. In the present report, we asked whether variation at MTHFR (677C-->T) or MTRR (66A-->G) might be associated with human trisomies other than trisomy 21. We analyzed maternal polymorphisms at MTHFR and MTRR in 93 cases of sex-chromosome trisomy, 44 cases of trisomy 18, and 158 cases of autosomal trisomies 2, 7, 10, 13, 14, 15, 16, 18, or 22, and compared the distributions of genotypes to those of control populations. We observed a significant increase in the MTHFR polymorphism in mothers of trisomy 18 conceptuses but were unable to identify any other significant associations. Overall, our observations suggest that, at least for the sex chromosomes and for a combined set of autosomal trisomies, polymorphisms in the folate pathway are not a significant contributor to human meiotic nondisjunction.
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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.