Journal
BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
Volume 85, Issue 4, Pages 314-321Publisher
WILEY
DOI: 10.1002/bdra.20542
Keywords
Folic acid; neural tube defects; folate metabolic pathway; mouse models; nucleotide biosynthesis; methylation
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Funding
- NRSA [NS059562]
- WCMC-THMRI initiative
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Despite two decades of research since Smithells and colleagues began exploring its benefits, the mechanisms through which folic acid supplementation supports neural tube closure and early embryonic development are still unclear. The greatest progress toward a molecular-genetic understanding of folate effects on neural tube defect (NTD) pathogenesis has come from animal models. The number of NTD-associated mouse mutants accumulated and studied over the past decade has illuminated the complexity of both genetic factors contributing to NTDs and also NTD-gene interactions with folate metabolism. This article discusses insights gained from mouse models into how folate supplementation impacts neurulation. A case is made for renewed efforts to systematically screen the folate responsiveness of the scores of NTD-associated mouse mutations now identified. Designed after Crooked tail, supplementation studies of additional mouse mutants could build the molecular network maps that will ultimately enable tailoring of therapeutic regimens to individual families. Birth Defects Research (Part A) 85:314-321, 2009. (C) 2008 Wiley-Liss, Inc.
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