Autism spectrum disorder (ASD) is an early development-related heterogeneous neuropsychiatric disorder with high prevalence and yet no cure. ASD display high genetic heterogenesis and may be caused by both inheritable and do novo gene variations. Thanks to the development of ASD animal models, ranging from rodents to primates, people are starting to unveil the underlying pathogenesis of ASD. Cumulative evidence suggests convergence in altered neural transmission and circuitry modulation in these ASD models. For example, altered excitation/inhibition ratio of neural transmission in multiple brain regions are commonly observed in several lines of autistic mice models. Several mechanisms have been identified underlying the impaired neural circuitry, such as disruption of transcriptional regulation, protein synthesis and degradation, synaptic cytoskeletal organization and receptor synaptic targeting. However, considerable amount of work is still required to identify specific molecular events, by regulating particular neural circuits, in controlling different autism-related behaviors such as social and stereotyped behaviors.
With this Research Topic, we are seeking contributions exploring molecular pathophysiology in autism and the potential therapeutic interventions based on such findings. We will not only focus on the evidence in the above-mentioned cellular events but also on alterations in signaling pathways leading to chaos in neuronal development, local circuitry transmission and circuitry formation in certain brain regions. The scope of this collection of articles is not limited to neurons, glia or microbiome as the interaction or functional modulation among those are also of interest. Studies could be carried out by various approaches such as high throughput screening, biochemistry, electrophysiology, optogenetic, pharmacology. Specific attention will be given to studies that demonstrate the relationship between abnormal signaling and behavioral features of autism. Papers illustrating basic mechanisms in new animal models will also be heavily weighted.
Autism spectrum disorder (ASD) is an early development-related heterogeneous neuropsychiatric disorder with high prevalence and yet no cure. ASD display high genetic heterogenesis and may be caused by both inheritable and do novo gene variations. Thanks to the development of ASD animal models, ranging from rodents to primates, people are starting to unveil the underlying pathogenesis of ASD. Cumulative evidence suggests convergence in altered neural transmission and circuitry modulation in these ASD models. For example, altered excitation/inhibition ratio of neural transmission in multiple brain regions are commonly observed in several lines of autistic mice models. Several mechanisms have been identified underlying the impaired neural circuitry, such as disruption of transcriptional regulation, protein synthesis and degradation, synaptic cytoskeletal organization and receptor synaptic targeting. However, considerable amount of work is still required to identify specific molecular events, by regulating particular neural circuits, in controlling different autism-related behaviors such as social and stereotyped behaviors.
With this Research Topic, we are seeking contributions exploring molecular pathophysiology in autism and the potential therapeutic interventions based on such findings. We will not only focus on the evidence in the above-mentioned cellular events but also on alterations in signaling pathways leading to chaos in neuronal development, local circuitry transmission and circuitry formation in certain brain regions. The scope of this collection of articles is not limited to neurons, glia or microbiome as the interaction or functional modulation among those are also of interest. Studies could be carried out by various approaches such as high throughput screening, biochemistry, electrophysiology, optogenetic, pharmacology. Specific attention will be given to studies that demonstrate the relationship between abnormal signaling and behavioral features of autism. Papers illustrating basic mechanisms in new animal models will also be heavily weighted.
