University of California, Los Angeles
Weatherstone Predoctoral Fellowship
This proposal is based on an overarching hypothesis that neural connectivity is disrupted in infants at high risk for ASD, with the biggest differences found in those infants who have delayed or atypical development. The earlier we can identify these differences in brain patterns, the earlier we can begin to monitor and even intervene with environmental enrichment.
My study will focus on quantitative electrophysiological measures of neural connectivity, with focus on whole brain and regional coherence in an ongoing longitudinal study of brain development in familial risk infants.
Research has made clear that infants with an older sibling with ASD are at heightened risk for the condition, with rates approaching 20 percent. These “baby sibs” provide a valuable opportunity to study the earliest markers of atypical brain development and risk for ASD.
This study has two primary aims:
1) to identify the earliest age at which resting state functional connectivity differs between infants with familial risk for autism and low risk infants using EEG; and
2) to examine whether resting state functional connectivity in early infancy predicts language and ASD severity at 36 months.
This study will identify early biomarkers that will guide earlier monitoring of familial risk infants and help us understand trajectories to both typical and atypical development, with the goal of attenuating and even preventing the delays that precede an autism diagnosis.
Developmental Biology, Broader Autism Phenotype, Regression/ Developmental Trajectory, Biomarker, Electrophysiology, EEG, Biology, Screening/ Diagnosis/ Phenotyping, Infants (0-17 Months), Toddlers (18 Months-3 Years), Individuals At Risk For ASD