|Project Title||Principal Investigator||Institution|
|High content screens of neuronal development for autism research||Halpain, Shelley||University of California, San Diego|
|Neurogenomics in a model for procedural learning||Hilliard, Austin||University of California, Los Angeles|
|Preclinical testing of novel oxytocin receptor activators in models of autism phenotypes||Jarstfer, Michael||University of North Carolina at Chapel Hill|
|Functional study of synaptic scaffold protein SHANK3 and autism mouse model||Jiang, Yong-Hui||Duke University|
|Investigating the effects of chromosome 22q11.2 deletions||Karayiorgou, Maria||Columbia University|
|Control of synaptic protein synthesis in the pathogenesis and therapy of autism||Kelleher, Raymond||Massachusetts General Hospital|
|Animal model of speech sound processing in autism||Kilgard, Michael||University of Texas at Dallas|
|Shank3 mutant characterization in vivo||Kouser, Mehreen||University of Texas Southwestern Medical Center|
|Behavioral and physiological consequences of disrupted Met signaling||Levitt, Pat||University of Southern California|
|The genetics of restricted, repetitive behavior: An inbred mouse model||Lewis, Mark||University of Florida|
|Serotonin, corpus callosum, and autism||Lin, Rick||University of Mississippi Medical Center|
|Interaction between MEF2 and MECP2 in the pathogenesis of autism spectrum disorders - 1||Lipton, Stuart||Burnham Institute|
|Using Drosophila to model the synaptic function of the autism-linked NHE9||Littleton, J. Troy||Massachusetts Institute of Technology|
|Insight into MeCP2 function raises therapeutic possibilities for Rett syndrome||Lomvardas, Stavros||University of California, San Francisco|
|Autism iPSCs for studying function and dysfunction in human neural development||Loring, Jeanne||The Scripps Research Institute|
|Evaluation of altered fatty acid metabolism via gas chromatography/mass spectroscopy and time-of-flight secondary ion mass spectroscopy imaging in the propionic acid rat model of autism spectrum disorders||MacFabe, Derrick||University of Western Ontario|
|Neuropharmacology of motivation and reinforcement in mouse models of autistic spectrum disorders||Malanga, C.J.||University of North Carolina School of Medicine|
|NrCAM, a candidate susceptibility gene for visual processing deficits in autism||Maness, Patricia||University of North Carolina at Chapel Hill|
|Synaptic deficits of iPS cell-derived neurons from patients with autism||Mao, Rong||Stanford University|
|Modeling and pharmacologic treatment of autism spectrum disorders in Drosophila||McDonald, Thomas||Albert Einstein College of Medicine of Yeshiva University|
|A mouse knock-in model for ENGRAILED 2 autism susceptibility||Millonig, James||University of Medicine & Dentistry of New Jersey|
|16p11.2: defining the gene(s) responsible||Mills, Alea||Cold Spring Harbor Laboratory|
|Novel models to define the genetic basis of autism||Mills, Alea||Cold Spring Harbor Laboratory|
|Characterization of a novel mouse model of restricted repetitive behaviors||Moy, Sheryl||University of North Carolina at Chapel Hill|
|Preclinical testing of novel oxytocin receptor activators in models of autism phenotypes||Moy, Sheryl||University of North Carolina at Chapel Hill|
|IACC Strategic Plan Objective||2008||2009||2010||2011||2012||Total|
|Standardize and validate at least 20 model systems (e.g., cellular and/or animal) that replicate features of ASD and will allow identification of specific molecular targets or neural circuits amenable to existing or new interventions by 2012.
IACC Recommended Budget: $75,000,000 over 5 years
|4.S.B. Funding: The recommended budget was met. Significantly more than the recommended minimum budget was allocated to projects specific to this objective.
Progress: More than 90 projects were supported to develop animal models.
Remaining Gaps, Needs, and Opportunities: Planning Group members discussed whether the amount of investment in this area is appropriate when compared to investments in clinical trials and other later stage studies. Invited experts suggested that the current stage of scientific research in ASD requires pre-clinical research to identify targets from animal and cellular models. Similar to cancer treatment development pathways, which spanned 20-30 years, research in ASD must invest in model systems to understand the fundamental biology from which translation to the clinic can be built. The translational validity of research in non-human animals cannot be determined until human trials are conducted, thus the need for rapid progress to clinical studies in humans is important.