Epigenetic alterations underlying the neurodevelopmental aspects of Autism Spectrum Disorders (ASD) are emerging as important risk factors for disease pathogenesis. These influences present the case that gene expressions may sustain alterations at higher levels of complexity than modifications in the DNA sequence. Part-and-parcel and central to this notion, the phenomenon involves essential environmental impacting upon the gametes before conception. Genomic imprinting may be described as a process of silencing genes through DNA methylation with major effects upon placental biology, brain and functional development and the etiopathogenesis of neuropsychiatric disorders.
It offers an epigenetic phenomenon through which some genes may be expressed in a manner that presents parent-of-originspecificity and may be viewed as an essential mechanism for gene regulation based on chemical modifications of DNA and histone proteins. If the allele inherited from the father is imprinted, it is thereby silenced, and only the allele from the mother is expressed. If the allele from the mother is imprinted, then only the allele from the father is expressed. Forms of genomic imprinting have been demonstrated in fungi, plants and mammals with over 150 imprinted in laboratory rodents.