An apparent link between the methylation status and gene transcription levels has led to the speculation that alterations in the methylation pattern (epimutations) might contribute to altered gene expression. Such epimutations are thought to occur upon exposure to environmental risk factors, including early developmental stress. Since early embryos seem to be particularly sensitive to epimutations [193, 194], this factor should be considered for the aetiology of neurodevelopmental disorders. For instance, epigenetic alterations are responsible for a number of neurodevelopmental disorders with single-gene defects, such as Rett Syndrome, ICF Syndrome, Fragile X Syndrome and ATR-X Syndrome [195-198]. A role for DNA methylation has also been proposed in connection with complex neurodevelopmental disorders. For example, spina bifida can be caused by a lack of folate [reviewed in 199], a compound needed for the generation of S-adenosylmethionine (SAM) that donates the methyl group 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
