Maria T Lázaro1, Peyman Golshani. 1. Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, Calofornia, USA.
Abstract
PURPOSE OF REVIEW: This review discusses the ways that rodent models of autism spectrum disorders (ASDs) have been used to gain critical information about convergent molecular pathways, the mechanisms underlying altered microcircuit structure and function, and as a screen for potential cutting edge-treatments for ASDs. RECENT FINDINGS: There is convergent evidence that impaired developmental pruning of connections may be a common finding among several mouse models of ASDs. Recent studies have uncovered impaired autophagy by pathological mTOR activation as a potential contributor to microcircuit dysfunction and behavior. ASD-related disinhibition and exaggerated synaptic plasticity in multiple distinct circuits in cortex and reward circuits in striatum also contribute to social dysfunction and repetitive behaviors. New exciting molecular therapeutic techniques have reversed cognitive deficits in models of ASD, indicating that mouse models could be used for preclinical translational studies of new treatments. SUMMARY: Rodent models of ASDs coupled to new emerging technologies for genome editing, cell-specific functional and structural imaging, and neuronal activity manipulation will yield critical insights into ASD pathogenesis and fuel the emergence of new treatments.
PURPOSE OF REVIEW: This review discusses the ways that rodent models of autism spectrum disorders (ASDs) have been used to gain critical information about convergent molecular pathways, the mechanisms underlying altered microcircuit structure and function, and as a screen for potential cutting edge-treatments for ASDs. RECENT FINDINGS: There is convergent evidence that impaired developmental pruning of connections may be a common finding among several mouse models of ASDs. Recent studies have uncovered impaired autophagy by pathological mTOR activation as a potential contributor to microcircuit dysfunction and behavior. ASD-related disinhibition and exaggerated synaptic plasticity in multiple distinct circuits in cortex and reward circuits in striatum also contribute to social dysfunction and repetitive behaviors. New exciting molecular therapeutic techniques have reversed cognitive deficits in models of ASD, indicating that mouse models could be used for preclinical translational studies of new treatments. SUMMARY: Rodent models of ASDs coupled to new emerging technologies for genome editing, cell-specific functional and structural imaging, and neuronal activity manipulation will yield critical insights into ASD pathogenesis and fuel the emergence of new treatments.
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