Yoram Bonneh will investigate basic cognitive skills related to receptive language and reading in minimally verbal individuals with autism spectrum disorder via the analysis of involuntary eye movements in response to pictures, text and sound. These studies are intended to test the hypothesis that core action-control deficits for voluntary or intentional behavior may result in a significant gap between the observed and actual cognitive abilities in such individuals.

Using new magnetic resonance imaging techniques and analysis approaches to identify focal cortical dysplasias (FCDs), Ruth Carper aims to determine whether FCDs occur more frequently in individuals with ASDs than is currently appreciated and to understand what effects FCDs have on cognition and behavior in ASD.

Geoffrey Goodhill will address how the early development of neural sensory circuits is altered in autism spectrum disorders, using a zebrafish model of fragile X syndrome to examine alterations in the developmental patterns of neural activity and their relationship to changes in visually driven behaviors.

Mark Zylka will test the hypothesis that exposure to environmental risk factors for ASD amplifies the effects of genetic risk factors, by assessing the effects of prenatal exposure to a pyrethroid pesticide in a genetic mouse model of ASD (Chd8+/- mice). The results of this research could identify an avoidable environmental risk for a common genetic subtype of autism.

Using a mouse model of fragile X syndrome, Hye Young Lee aims to understand the molecular mechanisms by which FMRP causes microglia dysfunction and to elucidate the effects of Fmr1 mutations on microglia-neuron communication under basal conditions as well as after neuroinflammation.

Using a battery of cutting-edge approaches, Song-Hai Shi will investigate lineage-dependent, precise, local and long-range cortical neuron circuit assembly in the Fmr1 knockout mouse model of fragile X syndrome.

Sensory experience and learning refine circuits through elimination of excitatory synapses, a process that depends on activity-driven transcription control and that is deficient in humans with ASD and mouse ASD models. Kimberly Huber and Tae-Kyung Kim will determine the role of ASD-linked epigenetic factors in activity-driven synapse elimination using mouse model systems and identify their gene regulatory networks at the single neuron level.

Mark Blumberg will perform behavioral and neurophysiological assessments in 16p11.2 deletion mice to determine whether the early sensorimotor and sleep disturbances observed in autism have a common link.

Anna Penn will assess cerebellar white matter and circuitry alterations in a new mouse model that lacks placental expression of the neurosteroid allopregnanolone. These changes will be compared to those observed in mouse models of ASD risk genes to identify common circuits that are fundamental to the expression of behavioral deficits relevant to ASD.

Markus Meister will detect and analyze abnormal circuit functions of the retina in mouse models of autism in order to draw links between autism genes and neuronal circuit processing.