| Literature DB >> 32209454 |
Whitney E Heavner1, Stephen E P Smith2.
Abstract
Genes that are mutated in Autism Spectrum Disorders (ASD) can be classified broadly as either synaptic or developmental. But what if this is a false distinction? A recent spate of publications has provided evidence for developmental mechanisms that rely on neural activity for proper cortical development. Conversely, a growing body of evidence indicates a role for developmental mechanisms, particularly chromatin remodeling, during learning or in response to neural activity. Here, we review these recent publications and propose a model in which genes that confer ASD risk operate in signal transduction networks critical for both cortical development and synaptic homeostasis.Entities:
Keywords: E/I balance; autism; chromatin; cortical development; genetics; genomics; neural activity; neuron migration; precision medicine; sensory integration; signal transduction; synapse
Year: 2020 PMID: 32209454 PMCID: PMC7101276 DOI: 10.1016/j.tins.2020.01.009
Source DB: PubMed Journal: Trends Neurosci ISSN: 0166-2236 Impact factor: 13.837