The aim of this topic is two fold: 1) to deal with cutting edge research on specific components associated with ASD (Autism Spectrum Disorders) such as repetitive behaviors, sensory abnormalities and self injury and 2) to disseminate the advances in the neurobiology of ASD, with a specific focus on the cellular and molecular alterations that affect neural development in a number preclinical mouse models of these disorders.
Restricted and repetitive behaviours (RRBs) are core features of ASD and encompass behaviours and preoccupations which are characteristically restricted and inflexible, such as repetitive language or movements, insistence on the same routines, and circumscribed interests. These clinical manifestations are correlated and frequently occur together in the same individual. Sensory processing abnormalities are often associated with RRBs. Treatment of RRB and self injury as the more dangerous expression of this continuum are in urgent need of new empirical data.
Therapeutic updates will be dealt with including pharmacological and behavioral intervention. In spite of the limited progress in pharmacological options for ASD a consistent number of experimental trials have been carried out recently. In parallel controlled studies on various type of behavioral intervention in ASD are on the increase and will contribute, together with targeted pharmacological therapies, to develop novel evidence-based, tailored interventions.
In the recent years, research on the neurobiological basis of ASD has made a considerable progress, leading to the identification of several genes and signaling pathways associated to ASD pathogenesis. Nevertheless, our understanding of ASD complexity of ASD remains obscure, and needs further investigation. The second issue of this topic is therefore to provide an overview of current studies performed on both human and mouse models, which highlight the importance of investigating the molecular mechanisms underlying ASD pathogenesis. Genomic studies allowed to identify genetic similarities between ASD and other disorders such as epilepsy and schizophrenia, strengthening the notion that ASD has strong neurodevelopmental component. Several studies performed on appropriate preclinical mouse models confirmed this hypothesis, highlighting the importance of altered developmental synaptic function and GABAergic neurotransmission in ASD. In addition, in vitro studies on induced pluripotent stem cells (iPSCs) derived from ASD patients contributed to identify novel molecular mechanisms and therapeutic targets.
This Research Topic is meant to be the follow up of the previous one: New treatment perspectives in ASD recently published in Child and Neurodevelopmental Psychiatry and hope to fill the gaps of the many unresolved issues in ASD.
The aim of this topic is two fold: 1) to deal with cutting edge research on specific components associated with ASD (Autism Spectrum Disorders) such as repetitive behaviors, sensory abnormalities and self injury and 2) to disseminate the advances in the neurobiology of ASD, with a specific focus on the cellular and molecular alterations that affect neural development in a number preclinical mouse models of these disorders.
Restricted and repetitive behaviours (RRBs) are core features of ASD and encompass behaviours and preoccupations which are characteristically restricted and inflexible, such as repetitive language or movements, insistence on the same routines, and circumscribed interests. These clinical manifestations are correlated and frequently occur together in the same individual. Sensory processing abnormalities are often associated with RRBs. Treatment of RRB and self injury as the more dangerous expression of this continuum are in urgent need of new empirical data.
Therapeutic updates will be dealt with including pharmacological and behavioral intervention. In spite of the limited progress in pharmacological options for ASD a consistent number of experimental trials have been carried out recently. In parallel controlled studies on various type of behavioral intervention in ASD are on the increase and will contribute, together with targeted pharmacological therapies, to develop novel evidence-based, tailored interventions.
In the recent years, research on the neurobiological basis of ASD has made a considerable progress, leading to the identification of several genes and signaling pathways associated to ASD pathogenesis. Nevertheless, our understanding of ASD complexity of ASD remains obscure, and needs further investigation. The second issue of this topic is therefore to provide an overview of current studies performed on both human and mouse models, which highlight the importance of investigating the molecular mechanisms underlying ASD pathogenesis. Genomic studies allowed to identify genetic similarities between ASD and other disorders such as epilepsy and schizophrenia, strengthening the notion that ASD has strong neurodevelopmental component. Several studies performed on appropriate preclinical mouse models confirmed this hypothesis, highlighting the importance of altered developmental synaptic function and GABAergic neurotransmission in ASD. In addition, in vitro studies on induced pluripotent stem cells (iPSCs) derived from ASD patients contributed to identify novel molecular mechanisms and therapeutic targets.
This Research Topic is meant to be the follow up of the previous one: New treatment perspectives in ASD recently published in Child and Neurodevelopmental Psychiatry and hope to fill the gaps of the many unresolved issues in ASD.