Brian PopkoUniversity of Chicago, USA F1000 Faculty Member (since 02 August 2004)
Professor, Committee on Genetics, Genomics & Systems Biology, Department of Molecular Biosciences, University of Chicago
Pennsylvania State University, Microbiology, BS, 1980
University of Miami School of Medicine, Microbiology, PhD, 1984
My laboratory takes a molecular genetic approach to obtain a better understanding of the normal function, as well as dysfunction, of the nervous system, primarily through the use of mouse models. Our ability to manipulate the mouse genome has become increasingly sophisticated, such that intricate mouse models can be generated. The detailed analyses of transgenic models of disease have proven to be extremely valuable tools for understanding human disorders. These efforts have resulted in the identification of genes responsible for human genetic disorders, and the generation of authentic models of human diseases. Additionally, the 'phenocopying' of particular traits of a syndrome have proven to be very useful. Mouse models of Alzheimer's disease, Creutzfeldt-Jakob disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis have all proven extremely informative in our current understanding of these disorders, as well as in the design of therapeutic approaches.
Our laboratory is focusing considerable effort on the generation and analysis of mouse models of peripheral neuropathies with the expectation that they will provide similar benefit. In particular, we are interested in disorders that alter the interactions of myelinating glial cells with axons. Axo-glial interactions play a critical role in the formation and maintenance of the nervous system, such that a disruption in these contacts results in severe neurological dysfunction. In the peripheral nervous system, the myelinating glia are the Schwann cells. Both heritable and environmental factors can damage Schwann cells, altering the peripheral nerve myelin sheath and resulting in peripheral neuropathies. In some cases, the damaging factors are heritable, such as in Charcot-Marie-Tooth disease, while others are acquired, as in Guillain-Barre syndrome, which results from an autoimmune response. Similarly, both genetic and environmental factors may disrupt normal axonal function. It is our goal to use the peripheral neuropathy mouse models to better understand the underlying molecular mechanisms that result in peripheral nerve disease, so that this knowledge and our models can be used to develop clinical treatments that serve to either protect neurons and Schwann cells against disease or aid in their recovery.
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