Neural Tube Defects and Folate

Neural Tube Defects and Folate

Neural tube defects (NTDs) are one of the severe congenital anomalies that cause by the failure of neurulation. Failure of fusion of the neural tube occurs around the 28th day after conception, when most women do not know they are pregnant.

NTDs in humans is multifactorial disorder; genetic and environmental effects.

Since 1960, scientists suggested that low folate status was important and vital risk factor for NTD. Studies are showed that the folic acid (0.36 mg dosage) supplement reduced the recurrence rate of NTDs from 5.9% to 0.5%. 

Folate is an essential water soluble B vitamin that is particularly from fruits and vegetables.

Neural tube defects (NTD) take place in one out of 1000 in the United States, and they are the second most common type of birth defect after congenital heart defects.

Folate and NTDs

1)     Folates connected to NTD risk through their bioavailability. . Inactivation of the gene FOLR1 coding for folate carrier’s proteins in neuroepithelial, neural crest and visceral endoderm cells cause neural tube defects

2)     Folate is nucleotide synthesis that may be related to NTD risk. The neural tube development require the synthesis of huge amounts of nucleotides in order to facilitate DNA replication due to their rapidly cell dividing.

3)     Adequate functioning of the methylation cycle is important for cranial neural tube closure. 

Refrences:

1)      Imbard A., Benoist j., Blom H. Neural Tube Defects, Folic Acid and Methylation. Int. J. Environ. Res. Public Health 2013, 10, 4352-4389.

2)      Stover, P.J.; Field, M.S. Trafficking of intracellular folates. Adv. Nutr. 2011, 2, 325–331.

3)       Imbard, A.; Smulders, Y.M.; Barto, R.; Smith, D.E.; Kok, R.M.; Jakobs, C.; Blom, H.J. Plasma choline and betaine correlate with serum folate, plasma S-adenosyl-methionine and S-adenosyl-homocysteine in healthy volunteers. Clin. Chem. Lab. Med. 2012, 51, 683–692.