Brian Popko, Ph.D.


  • Professor, Department of Neurology, Committee on Neurobiology, Committee on Molecular Medicine/MPMM
  • Associate Chair for Research, Dept. of Neurology
  • Director, Jack Miller Center for Peripheral Neuropathy 


Ph.D., University Miami, 1984


The University of Chicago
AB 510 / MC 2030
5841 South Maryland Ave. 
Chicago, Illinois 60637

Phone:  (773) 702-4953

Website (Dept. of Neurology)


My laboratory takes a molecular genetic approach to obtain a better understanding of the normal function, as well as dysfunction, of the nervous system.  We are particularly interested in the interactions between neuronal and glial cells, and the role that these interactions play in the development and function of the nervous system.  In pursuit of these interests, we take advantage of the increasingly sophisticated techniques available to mouse geneticists that allows us to generate intricate mouse models.

The generation and analysis of mouse models is central to my laboratory's line of inquiry. 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 better understanding 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 neurological disorders with the expectation that they will continue to provide substantial benefit.

In particular, we are exploiting techniques useful for the manipulation of the mouse genome that allow for the controlled activation or inactivation of predetermined genes in a spatially restricted manner.  We are using these approaches to express proteins, which are believed to be detrimental to the function of the CNS, in a regulated manner in specific brain cell types.  We are also inactivating specific genes in a regulated, cell-specific manner in an effort to further elucidate their function in the nervous system.  These powerful in vivo approaches will also likely assist us in our analysis of neurological disease processes.

My laboratory is particularly 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.  For example, focal immune-mediated demyelination of the central nervous system is the hallmark of multiple sclerosis and alterations to the peripheral nerve myelin sheath are the cause of the peripheral neuropathies Charcot-Marie-Tooth disease and Guillain-Barre syndrome.  The generation and analysis of mouse models of these and other neurological disorders will not only provide insight into the disease process, but will also make available model systems that will assist in the rational design of therapeutic strategies for these disorders.

Research Papers in PubMed