|Project Title||Principal Investigator||Institution|
|A mitochondrial etiology of autism||Wallace, Douglas||Children's Hospital of Philadelphia|
|Project 2: Immunological susceptibility of autism||Van de Water, Judy||University of California, Davis|
|Does mercury and neurotension induce mitochondrial DNA release from human mast cells and contribute to auto-immunity in ASD?||Theohardies, Theoharis||Tufts University|
|The effect of mercury and neuropeptide triggers on human mast cell release of neurotoxic molecules||Theohardies, Theoharis||Tufts University|
|Mechanisms of mitochondrial dysfunction in autism||Shoffner, John||Georgia State University|
|Environmentally induced oxidative stress and altered local brain thyroid horomone metabolism: relevance to autism?||Sajdel-Sulkowski, Elizabeth||Harvard Medical School; Brigham and Women's Hospital|
|A primate model of gut, immune, and CNS response to childhood vaccines||Sackett, Gene||University of Washington|
|EFRI- BSBA: Novel microsystems for manipulation and analysis of immune cells||Revzin, Alexander||University of California, Davis|
|Consequences of maternal antigen exposure on offspring immunity: An animal model of vertical tolerance||Rall, Glenn||The Fox Chase Cancer Center|
|Influence of the maternal immune response on the development of autism||Ponzio, Nicholas||University of Medicine & Dentistry of New Jersey|
|Influence of maternal cytokines during pregnancy on effector and regulatory T helper cells as etiological factors in autism||Ponzio, Nicholas||University of Medicine & Dentistry of New Jersey|
|Influence of maternal cytokines on activation of the innate immune system as a factor in the development of autism||Ponzio, Nicholas||University of Medicine & Dentistry of New Jersey|
|Gene-environment interactions in the pathogenesis of autism-like neurodevelopmental damage: A mouse model||Pletnikov, Mikhail||Johns Hopkins University School of Medicine|
|A non-human primate autism model based on maternal infection||Patterson, Paul||California Institute of Technology|
|A non-human primate autism model based on maternal immune activation||Patterson, Paul||University of California, Davis|
|Neurological diseases due to inborn errors of metabolism||Pascual, Juan||University of Texas Southwestern Medical Center|
|Maternal infection and autism: Impact of placental sufficiency and maternal inflammatory responses on fetal brain development||Palmer, Theo||Stanford University|
|Redox abnormalities as a vulnerability phenotype for autism and related alterations in CNS development||Noble, Mark||University of Rochester|
|Influence of oxidative stress on transcription and alternative splicing of methionine synthase in autism||Muratore, Christina||Northeastern University|
|Prostaglandins and cerebellum development||McCarthy, Margaret||University of Maryland, Baltimore|
|Immune molecules and cortical synaptogenesis: Possible implications for the pathogenesis of autism||McAllister, A. Kimberley||University of California, Davis|
|Maternal immune activation, cytokines, and the pathogenesis of autism||McAllister, A. Kimberley||University of California, Davis|
|Regulation of inflammatory Th17 cells in autism spectrum disorder||Littman, Dan||New York University School of Medicine|
|Redox abnormalities as a vulnerability phenotype for autism and related alterations in CNS development||James, Sandra||Arkansas Children's Hospital Research Institute|
|How does IL-6 mediate the development of autism-related behaviors?||Hsiao, Elaine||California Institute of Technology|
|IACC Strategic Plan Objective||2008||2009||2010||2011||2012||Total|
|Support at least four research projects to identify mechanisms of fever, metabolic and/or immune system interactions with the central nervous system that may influence ASD during prenatal-postnatal life by 2010 (Fever studies to be started by 2012).
IACC Recommended Budget: $9,800,000 over 4 years
|2.S.A. Funding: The recommended budget for this objective was met.
Progress: Many projects were funded in this area (approximately 20-30 per year), but the field is still developing, and emphasis on this objective should continue in the future. Scientific advances have been made in linking maternal innate immune function and immune-system challenge to aspects of ASD. Methodological advances in the field include the development of animal models for study of the role of the immune system in ASD and PET ligands for imaging microglial activation.
Remaining Gaps, Needs and Opportunities: There is a need for a well-designed, multi-site clinical study of clinical effects of fever and to develop standard measures of fever and behavioral/cognitive outcomes. Questions about fever could be integrated into funded epidemiological studies. There is also interest in further work on metabolic and mitochondrial issues, but in order for this work to be done, there is a need for validation and standardization of measures for assessment of oxidative stress and mitochondrial function. More guidance is needed on the key questions for this field to answer â a workshop to define these methodologies may be helpful. One of the key questions is to determine whether it is the body temperature associated with fever or some consequence of immune activation and production of the febrile state that leads to amelioration of cognitive function.