Tremendous strides have been made in determining the genetic basis of ASD, but we continue to struggle to understand the links from genes to cells to circuits to behavior. Loren Frank, Kevin Bender and David Kastner plan to study a rat model of ASD, Scn2a haploinsufficiency, at the cellular, systems and behavioral levels in an effort to understand how genetically driven changes in cellular properties drive systems-level changes in activity patterns and behavioral changes in the ability to learn and to adapt to new situations.

Problems falling and staying asleep are extremely prevalent in individuals with ASD and heavily affect quality of life, but the underlying mechanisms are poorly understood. In the current project, Lucia Peixoto plans to investigate the relationship between sleep, circadian rhythms, sleep deprivation and ASD in three human-relevant mouse models to better understand mechanisms and pave the way to targeted therapies and interventions in the future.

The ability to reciprocally cooperate with other individuals is affected in ASD. To better understand the neural basis of cooperative interaction and to discover novel ways to casually enhance them, Steve Chang, Anirvan Nandy and Monika Jadi plan to determine the neural codes used for altruistic and mutual cooperation in the orbitofrontal cortex and apply distinct brain stimulation protocols during naturalistic social interactions.

Altered sensory processing is a core and predictive feature of ASD but the underlying mechanisms remain poorly understood. By investigating neural information processing during impaired visual perception in Cntnap2 knockout mice, Bilal Haider’s team can begin building a detailed picture of how changes in neural circuits alter perception of the external sensory world.

Individuals with ASD perceive and experience the world differently compared to neurotypical individuals, but the brain mechanisms underlying these phenomena remain unknown. Adi Mizrahi plans to study the involvement of cortical feedback in these processes using behavioral, electrophysiological and anatomical studies in the 16p11.2 deletion mouse model.

Autism is a neurodevelopmental condition with a strong genetic basis, but a gap in knowledge exists between genetic and behavioral phenotypes due to a lack of neurophysiological explanation. To bridge the gap, Hiroki Asari aims to characterize and rescue changes in visual processing in autism model mice using causal experimental tools in modern systems neuroscience.

In this study, Elena Tenenbaum, Shafali Spurling Jeste and a team of researchers and clinicians, plan to capitalize on recent advances in remote administration of cognitive development tasks and computer vision software to pilot the Remote Infant Studies of Early Learning (RISE) Battery. This project represents a critical first step to increased understanding of early cognitive development in autism and has the potential to elucidate the foundational underpinnings of clinical heterogeneity in autism. This in turn will inform more targeted, developmentally relevant early intervention strategies for infants with atypical developmental trajectories.