About the Lab
Here at the Foss-Feig Lab, our research combines clinical assessments with brain-based methods, including EEG and MRI, to examine sensory and perceptual functioning in autism spectrum disorder (ASD). We also study the relation between ASD and other neurodevelopmental disorders, including schizophrenia and psychosis prodrome, as well as monogenic disorders with a prominent ASD phenotype.
Using multimodal neuroimaging (EEG, MRI), psychophysical testing, eye tracking, and targeted clinical assessments, our research investigates sensory and perceptual processing as they differ between autism spectrum disorder (ASD) and typical development. We also examine the convergence and divergence between ASD and other neurodevelopmental disorders, including schizophrenia, as well as relations between experimental effects and specific patterns of clinical symptoms within the broad ASD population and among individuals exhibiting known genetic mutations that contribute to an ASD phenotype.
Our work address the following central questions:
Mechanisms of sensory and perceptual processing alterations in ASD
Question 1: Mechanisms of sensory and perceptual processing alterations in ASD
Overlap between ASD and schizophrenia
Question 2: Overlap between ASD and schizophrenia
Genetics-first approach to understanding mechanisms and developing biomarkers for ASD
Question 3: Genetics-first approach to understanding mechanisms and developing biomarkers for ASD
In this line of research, we collaborate with colleagues at Seaver to explore several research avenues. First, how is brain functioning and behavior different in individuals with genetic disorders? How is sensory functioning impacted, and how do social and attentional symptoms present? Second, how do differences in brain functioning in those with genetic syndromes compare to those in individuals with ASD with unknown cause (“idiopathic ASD”)? Are there groups of individuals with idiopathic ASD whose behavior and brain functioning looks similar to that associated with a specific genetic disorder? If so, might this give us clues into neural alterations that are affecting a broader portion of individuals with ASD, even when we don’t know the specific cause? Third, can we develop biomarkers for ASD starting in genetic syndromes? Are there brain-based alterations that are reliable across time and individuals and that can easily be measured regardless of a child’s functioning level or the research or clinical setting? Do these markers help us know which children will benefit from a specific treatment? When we do treat children, do these biomarkers show change? Can this work inform biomarkers and treatment approaches for ASD more broadly?
Seaver Autism Center for Research and Treatment
Icahn School of Medicine at Mount Sinai
Department of Psychiatry
One Gustave L. Levy Place
New York, NY 10029
Telephone: (212) 241-0961