Jun 22, 2000

Hypothesis: folate-responsive neural tube defects and neurocristopathies

Teratology
Aśok C Antony, Deborah K Hansen

Abstract

What accounts for the wide spectrum of folate-responsive dysmorphogeneses? Both embryonic and fetal cells are entirely dependent on maternal folate to support their requirement for precisely timed proliferative bursts during gestation. Folate receptors (FRs) mediate transport into cells and are central to transplacental maternal-to-fetal folate transport. FRs are also critical for neural tube and neural crest development because recent murine "knock-out" and "knock-down" of FRs results in a high percentage of folate-responsive neural tube defects (NTDs) and neurocristopathies. Central to our hypothesis is the fact that folate deficiency is accompanied by a reduction in the proliferative capacity of highly mitotic neural tube or neural crest cells. Therefore, depending on when in pregnancy various cohorts of highly proliferative cells are deprived of folate, and the origin of the affected cells will determine the type of developmental dysmorphogenesis. Thus, selective folate deficiency in early pregnancy of only highly proliferative neural tube or neural crest cells predisposes to NTDs or gross dysmorphogenesis, respectively. Folate deficiency that compromises placental development will predispose to small-for-date babies due to...Continue Reading

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  • Citations37

Mentioned in this Paper

Embryo
Neurodegeneration Due To Cerebral Folate Transport Deficiency
Bone Diseases, Developmental
Neural Tube
Placentation
Iniencephaly
Hormone Receptors, Cell Surface
Murine
Knock-out
Atresia

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