
Dr. Gene J. Blatt received his Ph.D. from Thomas Jefferson University in 1985 for work on the topography of olivocerebellar projections to the cerebella of types of mutant mice. For the next two years he was a postdoctoral fellow at the Salk Institute studying the primate extrastriate visual system. He came to the Department of Anatomy and Neurobiology in 1987 initially as a Research Associate studying the projections of limbic system structures in a non-human primate, and then joining the faculty where he is currently an Associate Professor. For the past decade his research efforts have focused on the neurodevelopmental disorder autism studying the neuropathology and neurochemical alterations in the cerebellum, limbic system and cortex. The overall goal of the studies are to identify and quantify biomarkers for the disorder with the potential to improve pharmacotherapies in affected individuals. The initial autism ligand binding studies found that there was a decrease in the density of GABAA receptors and its benzodiazepine binding sites in the hippocampus of adult individuals with autism via postmortem analysis. Subsequently, similar changes in these receptors were demonstrated in the anterior and posterior cingulate cortices as well as the fusiform gyrus. Additional studies found alterations in serotonergic receptor subtypes including the 5-HT1a and 5-HT2a receptors in the same three cortical areas. Cytoarchitectural abnormalities were found in cingulate areas suggesting defects during development. Cerebellar studies found a variety of alterations in the GABAergic system. In situ hybridization found altered levels of key GABA synthesizing enzymes, GAD65 and GAD67, in Purkinje cells, stellate and basket cells and in a subpopulation of dentate neurons. Collectively, these studies suggest that there are underlying cellular and molecular abnormalities in areas that normally function in social-emotional behavior including face processing, learning and memory and motor/cognitive functions, many of which are abnormal in autism.