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Biography

Dr. Dong graduated from the Fourth Military Medical University in 1993 and earned his Ph.D. degree there in 1999. His Ph.D. research and thesis was conducted at the University of Southern California under the direction of Professors Larry Swanson and Gong Ju. In 2004, Dr. Dong joined the Allen Institute for Brain Sciences as one of the founder scientists and constructed a standard mouse brain atlas, the Allen Reference Atlas (published by Wiley). This atlas was the backbone for generating a genome-wide gene expression mouse brain atlas for the Allen Brain Atlas project (www.brain-map.org) and has been widely used internationally in the field of neuroscience. In 2006, Dr. Dong joined the University of California, Los Angeles as an Assistant Professor and initiated the NIMH funded the Mouse Connectome Project (MCP, www.MouseConnectome.org), which aims to construct a high resolution connectivity atlas of the whole mouse brain. Recently, Dr. Dong moved to USC as an Associate Professor. He continues to lead the MCP.

Abstract

Activity of a single brain structure alone typically is not sufficient to produce behavior. Instead, behaviors require the cooperative assembly of multiple neural circuits and networks. Therefore, in disease states, both individual structures and their projection sources and targets are affected. Such “connectopathies” have been implicated in neurological disorders such as Alzheimer’s Disease (AD). However, currently little is known about the neuroanatomical wiring in neurological disease models and how these pathological connections correspond to cognitive deficits. To address this question, our research group adopted a high-throughput connectomics approach to systematically characterize the early and advanced alterations of hippocampal-subicular neuronal networks in a mouse model of AD, which expresses nonmutant human Tau isoforms in the absence of mouse Tau isoforms (htau mice). We found that across the progression of the disease, compromised connections correlated with neuropathological hallmarks (i.e., neurofibrillary tangle) and cognitive-behavioral impairments in a hippocampal dependent contextual fear conditioning procedure. We hope our approach will provide a novel strategy for exploring diagnostic and prognostic fingerprints not only for AD, but also for other disconnection syndromes.

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