Is High Folic Acid Intake a Risk Factor for Autism?-A Review.

Folate is required for metabolic processes and neural development. Insuring its adequate levels for pregnant women through supplementation of grain-based foods with synthetic folic acid (FA) in order to prevent neural tube defects has been an ongoing public health initiative. However, because women are advised to take multivitamins containing FA before and throughout pregnancy, the supplementation together with natural dietary folates has led to a demographic with high and rising serum levels of unmetabolized FA.

Could folic acid influence growth cone motility during the development of neural connectivity?

Perinatal dietary supplementation, together with widespread fortification of grain-based foods with synthetic folic acid (FA) has resulted in rising concentrations of unmetabolized plasma FA in pregnant women. In a recently published study we reported on experiments in which we cultured dorsal root ganglia from chick embryos in a range of FA concentrations. We found that FA inhibited neurite extension, synaptogenesis, and growth cone motility.

Influence of Folic Acid on Neural Connectivity during Dorsal Root Ganglion Neurogenesis.

The vitamin folic acid (FA) is essential for DNA synthesis, repair and methylation, and for methionine synthesis. Although it is necessary for neural development, recent studies suggest a possible link between excess maternal supplemental FA intake and adverse interferences with single-carbon metabolism and neural development. Insufficient FA early in brain development can lead to failure of the neural tube closure, but the consequences of too much intake have not been fully investigated.

Xenopus development from late gastrulation to feeding tadpole in simulated microgravity.

Microgravity (microG) is known to influence cytoskeletal structure, but its effects on cell migration are not well understood. To examine the effects of altered gravity on neural crest cell (NCC) migration, we inserted Xenopus laevis embryos into two separate microG-simulating slow turning lateral vessels (STLVs) just before neurulation (stage 11-12), and exposed them until feeding stage (stage 45), when the jaws and branchial apparatus are fully functional. To evaluate apparatus-related artifacts, we used two different STLVs and a vibration control as well as a stationary control vessel.

Neural crest cell motility in valproic acid.

Neural crest cells (NCCs) exit the dorsal neural tube and migrate to sites where they form diverse tissues. Valproic acid (VPA) is an anticonvulsant drug that induces neural tube and related defects. Altered NCC migration and proliferation have been proposed as mechanisms of teratogenicity.