Meaburn and Jones will test causal paths between ASD genetic risk and disruptions in the brain systems underpinning social attention, and examine how candidate protective environmental factors might moderate genetic risk.

Tsai will delineate contributions of cerebellar dysfunction to autism-related behaviors in mice and assess benefits of cerebellar neuromodulation to treat these behaviors.

Individuals with autism frequently experience visceral pain, constipation and diarrhea, but the mechanisms underlying such gastrointestinal symptoms are poorly understood. In the current project, David Julius’ laboratory is focused on delineating the properties of enterochromaffin cells, the serotonin-producing epithelial cells of the gut that detect noxious agents, communicate with sensory nerve fibers and contribute to visceral pain

By integrating in vitro, ex vivo and in vivo techniques, Ori-McKenney will provide insight into how MNB/DYRK1a contributes to autism.

Frick previously demonstrated a link between BKCa channel dysfunction, neocortical hyperexcitability and sensory hypersensitivity in the Fmr1-/y model of ASD. Drawing on this work, Frick will explore the potential of channel agonists for the therapeutic correction of phenotypes associated neocortical hyperexcitability/sensory hypersensitivity in genetic mouse models of ASD.

This project aims to study pharmacological tools that enhance energy production efficiency in neurons as a way to enhance learning and memory in individuals with fragile X syndrome.

Yu will leverage genomic data from SPARK, SSC and other large ASD cohorts to catalog biallelic/recessive ASD mutations, analyze phenotypic correlates and provide novel mechanistic insights.

Choi proposes to use the MIA mouse model with a discrete, functionally relevant lesion in the primary somatosensory cortex to elucidate neural circuits that modulate ASD-associated behaviors.

Gu will assess the contribution of mtDNA mutations to ASD by examining whole-genome sequencing SSC data and using maternal and fetal samples collected in the Boston Birth Cohort.

Lukens and Zunder will utilize transcriptomics, mass cytometry and data-driven science to uncover cellular and molecular underpinnings of sex bias in an MIA model of autism.