This may partly explain the high incidence of NTDs and neurocognitive impairment among infants exposed to VPA in utero (Marsh et al, 2006). Secondly, AEDs or their metabolites may disrupt pathways regulating normal fetal development. For example, VPA disrupts the Wnt signalling pathway, which allows communication between the cell membrane and nucleus. Thirdly, several AEDs seem to cause teratogenicity by inhibiting folate metabolism. As a final example—studies suggest a number of other mechanisms—several AEDs may induce neural apoptosis, suppressing endogenous systems that protect nerves (Kluger and Meador, 2008).