Merck

Neural tube defects, folic acid and methylation.

International journal of environmental research and public health (2013-09-21)
Apolline Imbard, Jean-François Benoist, Henk J Blom
ABSTRACT

Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is established that folic acid supplementation decreases the prevalence of NTDs, which has led to national public health policies regarding folic acid. To date, animal studies have not provided sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs. However, several lines of evidence suggest that not only folates but also choline, B12 and methylation metabolisms are involved in NTDs. Decreased B12 vitamin and increased total choline or homocysteine in maternal blood have been shown to be associated with increased NTDs risk. Several polymorphisms of genes involved in these pathways have also been implicated in risk of development of NTDs. This raises the question whether supplementation with B12 vitamin, betaine or other methylation donors in addition to folic acid periconceptional supplementation will further reduce NTD risk. The objective of this article is to review the role of methylation metabolism in the onset of neural tube defects.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Folic acid, meets USP testing specifications
Sigma-Aldrich
Folic acid, ≥97%
Sigma-Aldrich
Folic acid, BioReagent, suitable for cell culture, suitable for insect cell culture, suitable for plant cell culture, ≥97%
Supelco
Folic acid, Pharmaceutical Secondary Standard; Certified Reference Material
Folic acid, European Pharmacopoeia (EP) Reference Standard
USP
Folic acid, United States Pharmacopeia (USP) Reference Standard