Most individuals with autism experience at least one form of hypersensitivity from the five senses. These alterations in sensory-related behaviors can lead to profound limitations on an individual’s ability to work, interact with family and participate in leisure activities. Furthermore, these atypical responses to otherwise normal sensory stimuli may be closely associated with the core symptoms of autism, such as social deficits and repetitive behaviors. Despite the importance of sensory abnormalities in the pathogenesis of autism, how the brains of individuals with autism receive information from the five senses at the subcortical level and how such information becomes transformed into aversive responses has not been investigated.
Seizures are an extreme outcome of excitatory-inhibitory imbalance and are the most common neurological complication in autism spectrum disorder (ASD). Seizures are even more common in syndromic forms of ASD such as Angelman syndrome. In the current project, Ben Philpot’s laboratory aims to identify the circuitry and protein pathways underlying seizures in a mouse model of Angelman syndrome, with the goal of identifying disease-modifying targets to treat seizures. The mechanistic insights yielded by these studies may further guide therapeutically oriented investigations of excitatory-inhibitory imbalance across the broader spectrum of ASDs.
The sensory and neural mechanisms that mediate social communication facilitating attachment and how they are affected in the context of autism spectrum disorder (ASD) are poorly understood. Prairie voles are small rodents that display long-term relationships between peers and mates. Devanand Manoli proposes to understand how specific mutations in two ASD risk genes, Shank3 and Scn2a, disrupt the processing of social cues, leading to the identification of brain regions that could inform targeted interventions to improve social communication in ASD.
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