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.
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