in the DNA methylation process. Also, some patients with depressive illness and schizophrenia display lower serum folate levels [200]. Animal models further provide evidence for a possible link between epigenetics and neurodevelopmental disorders. Following a diet with L-methionine, a precursor in the biosynthesis of SAM, the reeler mouse (a model for schizophrenia) showed increased promoter methylation of the reelin gene, reduced reelin expression and a declined prepulse inhibition of startle. These effects could subsequently be reversed by valproic acid, a mood-stabilizing drug used for treatment of epilepsy, bipolar disorder and schizophrenia [201]. In addition, the adult offspring of rat mothers that showed high licking and grooming (LG) and arched-back nursing (ABN) (two forms of maternal behaviour in the rat that serve as the basis for the individuals programming of the stress response) are less fearful, have a lower hypothalamic-pituitary-adrenal response to stress, and have a lower DNA methylation status in the promoter region of the glucocorticoid receptor gene when compared to the offspring of low-LG and -ABN mothers [202]. Thus, alterations in epigenetic profiles may contribute to the generation of complex neurodevelopmental disorders.
