The foundations of brain architecture are established early in life through a continuous series of dynamic interactions in which environmental conditions and personal experiences have a significant impact on how genetic predispositions are expressed. New scientific research shows that early social experiences can actually influence how genes are expressed. Thus, the old-school concepts that genes are "chiseled in stone" or that they alone determine development have been disproven.
Synaptic plasticity, specifically long-term potentiation and long-term depression, is thought to be the underlying cellular mechanism for learning and memory processes in the brain. About two decades ago a new concept was introduced, namely metaplasticity, which comprises changes that modify the properties of synaptic plasticity due to a priming or preconditioning event.
Over the last several years proteins involved in base excision repair (BER) have been implicated in active DNA demethylation. We review the literature supporting BER as a means of active DNA demethylation, and explain how the various components function and cooperate to remove the potentially most enduring means of epigenetic gene regulation. Recent evidence indicates that the same pathways implicated during periods of widespread DNA demethylation, such as the erasure of methyl marks in the paternal pronucleus soon after fertilization, are operational in post-mitotic neurons.
Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impaired social interactions, language deficits, as well as restrictive or repetitive behaviors. ASD is clinically heterogeneous with a complex etiopathogenesis which may be conceptualized as a dynamic interplay between heterogeneous environmental cues and predisposing genetic factors involving complex epigenetic mechanisms. Inherited and de novo copy number variants provide novel information regarding genes contributing to ASD.