UC Davis MIND Institute researchers to present on autism at AAAS Annual Meeting in Vancouver
Feb 18, 2012 - 5:00:00 AM
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LaSalle will discuss her recent research into a particular flame-retardant chemical persistent in the environment, and how genetically engineered autism mice exposed to the substance were less fertile and their offspring were smaller, less sociable and demonstrated marked deficits in learning and long-term memory, when compared with the offspring of normal unexposed mice.
By University of California - Davis Health System,
[RxPG] Two UC Davis MIND Institute researchers will lead a symposium on relationships between genetic, epigenetic and environmental influences on the development of autism in children during the American Association for the Advancement of Science (AAAS) Annual Meeting, Feb. 16 -18 in Vancouver, Canada.
The symposium, Autism: Genetic, Epigenetic and Environmental Factors Influencing Neural Networks, will be held Feb. 18. The researchers, both affiliated with the UC Davis MIND Institute, are Isaac Pessah, director of the UC Davis Children's Center for Environmental Health and Disease Prevention and a professor in the UC Davis School of Veterinary Medicine, and Janine LaSalle, professor in the Department of Medical Microbiology and Immunology and in the Rowe Program in Human Genetics.
A news briefing on the symposium will be held at 9 a.m. on Feb. 19 in Room 221 on the second Level of the Vancouver Convention Center.
Autism is a heterogeneous set of developmental disorders with complex etiologies. The goal of the symposium is to present a multidisciplinary perspective on how genetic, epigenetic and environmental factors can interact to promote autism risk. Other presenters will include symposium co-organizer Cindy Lawler of the National Institute of Environmental Health Sciences, Scott Selleck of Pennsylvania State University and Pat Leavitt of the University of Southern California.
Pessah, the symposium organizer, will address how understanding how low-level chemical exposures influence molecular, cellular and behavioral outcomes relevant to the development of autism will enlighten geneticists, neuroscientists and immunologists about autism's complex etiologies, and possibly yield novel intervention strategies. The inherent imbalances in neuronal connectivity in children at risk for autism are likely to provide the biological substrate for enhanced susceptibility to environmental triggers that are known to target signaling systems. He also will discuss how recent results from studies conducted by investigators at the UC Davis Center for Children's Environmental Health highlight examples of gene/environment interactions relevant to autism risk.
LaSalle will discuss her recent research into a particular flame-retardant chemical persistent in the environment, and how genetically engineered autism mice exposed to the substance were less fertile and their offspring were smaller, less sociable and demonstrated marked deficits in learning and long-term memory, when compared with the offspring of normal unexposed mice.
The research is the first to link genetics and epigenetics with exposure to a flame retardant chemical. Other findings of the research are that female offspring of mice exposed to BDE-47 spent half as much time interacting with other mice in a 10-minute sociability test when compared with controls. The reduced sociability in BDE-47 exposed females corresponded to reduced DNA methylation in females, regardless of genotype. In addition, genetic and environmental interaction effects in this study were specifically observed in females.
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