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The offspring also exhibited ASD-like behavioral deficits that were dose-dependently prevented by maternal folic acid supplementation from E1 to E12.5 (111), which was consistent with the lower prevalence of ASD that correlates with maternal folic acid supplementation ( Inhibition of Histone Deacetylase Two other mechanisms may also link in utero VPA exposure to ASD in offspring, although they seem less relevant to clinical effects: inhibition of histone deacetylase (HDAC) and activation of the mTORC1 signaling pathway

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