Prevention of neural tube defects: vitamins, enzymes and genes.
Neural tube defects can be prevented by folic acid, although the mechanism of this action is unclear. Studies of a series of folate-related enzymes have so far failed to pin-point the nature of the metabolic defect in the neurulation-stage embryo that is corrected by folic acid. Approximately 30% of neural tube defects appear resistant to folic acid and recent work in a mouse genetic model system suggests that administration of myo-inositol may be a complementary therapeutic option. The large number of mouse genes known to cause neural tube defects provide a starting point for identifying the genetic basis of the human defects.
Copp
A J
AJ
Neural Development Unit, University College London, UK. a.copp@ich.ucl.ac.uk
D013766:5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / Q000378:metabolism; D000818:Animals; D003541:Cystathionine beta-Synthase / Q000378:metabolism; D005260:Female; D005492:Folic Acid / Q000378:metabolism / Q000627:therapeutic use*; D006710:Homocysteine / Q000378:metabolism; D006801:Humans; D007294:Inositol / Q000627:therapeutic use; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D051379:Mice; D008818:Mice, Neurologic Mutants; D009436:Neural Tube Defects / Q000201:enzymology / Q000235:genetics* / Q000517:prevention & control*; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000378:metabolism; D011247:Pregnancy; D014815:Vitamins / Q000627:therapeutic use*
D014815:Vitamins; D006710:Homocysteine; D007294:Inositol; D005492:Folic Acid; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D013766:5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; D003541:Cystathionine beta-Synthase