title: What are the molecular mechanisms of neural tube defects?
abstract: Neural tube defects (NTDs) are some of the most common human malformations. The vast majority of NTDs can be prevented by the administration of folic acid; however, to date there has been no effective treatment of folic acid-resistant NTDs. A recent paper has confirmed an earlier report that the administration of inositol to the curly tail mutant mouse, which is a model of folate-resistant NTDs, can cure such defects. The molecular pathway by which this is achieved is thought to occur by the up-regulation of the retinoic acid receptor beta in the underlying hindgut endoderm, correcting a proliferation defect. However, alternative explanations also may account for NTDs.
authors.affiliation: Developmental Biology Research Centre, Randall Institute, London, United Kingdom. udli155@kcl.ac.uk
authors.forename: J
authors.initials: J
authors.lastname: Corcoran
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004351:Drug Resistance; D005260:Female; D005492:Folic Acid / Q000494:pharmacology; D006801:Humans; D007294:Inositol / Q000494:pharmacology; D051379:Mice; D008817:Mice, Mutant Strains; D009436:Neural Tube Defects / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control; D011247:Pregnancy; D018168:Receptors, Retinoic Acid / Q000235:genetics; D014212:Tretinoin / Q000502:physiology
chemical_list: D018168:Receptors, Retinoic Acid; C082925:retinoic acid receptor beta; D007294:Inositol; D014212:Tretinoin; D005492:Folic Acid