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Author Notes:

A. Klin: +1 404 785 5762. ami.klin@emory.edu

We wish to thank the families and children for their time and participation in our various studies reviewed here.

We also wish to thank Jessica Jones, Andrea Trubanova, Jeremy Borjon, Jenn Moriuchi, Kate Rice, Jessie Northrup, Laura Edwards, Jennings Xu, Anna Krasno, Casey Zampella, Kelley Knoch, David Lin, Katelin Carr, and Amanda Blank for their assistance in data collection and analysis; Peter Lewis, Jose Paredes, Philip Gorrindo, and Marilyn Ackermann for assistance in designing and building lab hardware and software; Gordon Ramsay and Courtney McCracken for discussions of data analysis and statistics; Irene Zilber, Amy Margolis, Daniela Blum, Martha Dye, Deanna Simeone, Amanda Smith, and Kerry O'Loughlin for project supervision, coordination, and data collection; Tammy Babitz for administrative support; and Kasia Chawarska, Celine Saulnier, Suzanne Macari, Rhea Paul, Amy Carney, Tina Goldsmith, Amanda Steiner, Grace Gengoux, Diane Goudreau, Erin Loring, James McGrath, and Abha Gupta for their contributions to the clinical characterization of the samples; and Chris Gunter for editing the manuscript.


Research Funding:

This work was supported by grants from the Simons Foundation and the National Institute of Mental Health (R01 MH083727; P50-MH100029).

Additional support was provided by the Marcus Foundation; the J.B. Whitehead Foundation; and the Georgia Research Alliance.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Behavioral Sciences
  • Neurosciences
  • Neurosciences & Neurology
  • Autism
  • Autism spectrum disorders
  • Social visual engagement
  • Biological motion
  • Eye fixation
  • Infancy
  • Prodromal
  • Pathogenesis
  • Visual imprinting
  • Epigenetics

Social visual engagement in infants and toddlers with autism: Early developmental transitions and a model of pathogenesis


Journal Title:

Neuroscience and Biobehavioral Reviews


Volume 50


, Pages 189-203

Type of Work:

Article | Post-print: After Peer Review


Efforts to determine and understand the causes of autism are currently hampered by a large disconnect between recent molecular genetics findings that are associated with the condition and the core behavioral symptoms that define the condition. In this perspective piece, we propose a systems biology framework to bridge that gap between genes and symptoms. The framework focuses on basic mechanisms of socialization that are highly-conserved in evolution and are early-emerging in development. By conceiving of these basic mechanisms of socialization as quantitative endophenotypes, we hope to connect genes and behavior in autism through integrative studies of neurodevelopmental, behavioral, and epigenetic changes. These changes both lead to and are led by the accomplishment of specific social adaptive tasks in a typical infant's life. However, based on recent research that indicates that infants later diagnosed with autism fail to accomplish at least some of these tasks, we suggest that a narrow developmental period, spanning critical transitions from reflexive, subcortically-controlled visual behavior to interactional, cortically-controlled and social visual behavior be prioritized for future study. Mapping epigenetic, neural, and behavioral changes that both drive and are driven by these early transitions may shed a bright light on the pathogenesis of autism.

Copyright information:

© 2014 Elsevier Ltd.All rights reserved

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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