Miriam Rosenberg-Lee, PhD
Assistant Professor of Psychology
SASN, Rutgers-Newark

Thurs, Nov 19 (1.50 PM – 2.10 PM)

The Neural Basis of Cognitive Strengths in Autism
Autism spectrum disorders (ASD) are characterized by difficulties in social communication and repetitive and restrictive behaviors. Yet, the disorder is often accompanied by remarkable cognitive strengths in domains such as memory, spatial reasoning and musical ability. Understanding the neural basis of spared and enhanced abilities in ASD has the potential to elucidate mechanisms underlying both strengths and weakness in this population. Moreover, cultivating strengths, particularly in academic domains, like mathematics and reading, can contribute to improving life outcomes and supporting financial independence. Here, I present work examining enhanced arithmetic and word reading performance in children and college students with ASD. In both cases, reorganization of high-level visual processing areas in inferotemporal cortex (among other regions) underpinned these strengths. Further, these results point to mastery of symbolic systems, like letters and numbers, as a particularly potent learning modality in autism, but perhaps at a cost to other complex visual stimuli, such as faces.

Emanuel DiCicco-Bloom, MD
Professor of Neuroscience & Cell Biology

Thurs, Nov 19 (2.30 PM – 2.50 PM)

Defects in mTOR Signaling Mediate Common Neurite and Cell Migration Defects in both Idiopathic and 16p11.2 Autism Neural Precursor Cells
Autism spectrum disorder (ASD) is defined by common behavioral characteristics, raising the possibility of shared pathogenic mechanisms. Yet, vast clinical and etiological heterogeneity suggests there may also be personalized phenotypes. Surprisingly, our iPSC studies find that six individuals from two distinct ASD-subtypes, idiopathic (I-ASD) and CNV 16p11.2 deletion (16pDel), have common reductions in neural precursor cell (NPC) neurite outgrowth and migration, even though DNA sequencing demonstrates no genetic overlap, and growth factor responses reveal subtype-specific impairments. To identify signaling defects that may contribute to these developmental defects, an unbiased phospho (P)-proteomic screen was performed. Surprisingly, despite the genetic heterogeneity, numerous shared P-peptides were identified between the autism subtypes including the mTOR pathway. mTOR signaling alterations were confirmed in all NPCs across both ASD-subtypes, and mTOR modulation rescued phenotypes in ASD and reproduced autism defects in controls. Thus, our studies demonstrate that distinct non-overlapping genetic variants converge on mTOR signaling defects that mediate consistent neurite and cell migration defects in two distinct ASD subtypes.