What are the molecular mechanisms of neural tube defects?
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.
Corcoran
J
J
Developmental Biology Research Centre, Randall Institute, London, United Kingdom. udli155@kcl.ac.uk
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
D018168:Receptors, Retinoic Acid; C082925:retinoic acid receptor beta; D007294:Inositol; D014212:Tretinoin; D005492:Folic Acid