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National Institutes of Health U.S. Department of Health and Human Services - National Institutes of Health
National Center for Research Resources National Center for Research Resources

Jason C. Bartz, Ph.D.

Department of Medical Microbiology and Immunology
2500 California Plaza
Creighton University
Omaha, NE 68178
Tele: (402) 280-1811
Fax: (402) 280-1875
e-mail: jbartz@creighton.edu

Research Interests

Prion diseases are a group of fatal neurodegenerative diseases that affect humans (e.g. Creutzfeldt-Jacob disease) and animals (e.g. chronic wasting disease). Prion diseases have long subclinical incubation periods of months to decades with a short clinical phase that is characterized by the onset of behavioral, cognitive or motor deficits. Deposition of the abnormal isoform of the prion protein, PrPSc is pathognomonic for prion diseases and its deposition in the central nervous system (CNS) results in neuronal loss and onset of clinical symptoms. PrPSc is an amyloid protein that is resistant to proteolytic degradation and is postranslationally derived from the protease sensitive non-amyloid host encoded prion protein, PrPC. Outside of the CNS, PrPSc deposition occurs in the peripheral nervous system and secondary lymphoreticular system (LRS) tissues such as spleen and lymph nodes. All prion diseases of animals and a majority of prion diseases in humans are due to prion exposure by a peripheral route (e.g. ingestion). Details of the mechanism(s) of prion transport to the CNS are poorly understood. To better define prion transport to the CNS we are investigating three areas of prion pathogenesis. First, we are exploring alternative routes of prion entry into the host in an attempt to better define the possible routes that prions can gain access to the CNS. Second, we are investigating the role of the innate immune system in processing and transport of prions to secondary LRS tissues. Finally, we are interested in factors that influence susceptibility of neurons to prion infection and/or replication. The understanding of routes and mechanisms of prion transport will enhance the future development of therapeutic interventions to prevent prion spread to the CNS.

Selected Publications

McKenzie, D., Bartz, J. and Aiken, J. (1998). A molecular basis for transmissible spongiform encephalopathy agent strain differences.  Bulletin de l'Institut Pasteur 96, 35-47. 

McKenzie, D., Bartz, J., Mirwald, J., Olander, D.,  Marsh, R. and Aiken, J.  (1998).  Reversibility of scrapie inactivation is enhanced by copper.  Journal of Biological Chemistry 273, 25545-25547. 

Bartz, J.C., Marsh, R.F., McKenzie, D.M. and Aiken, J.M.  (1998).  The host range of chronic wasting disease is altered upon passage in ferrets.  Virology. 251, 297-301. 

Bartz, J.C., Bessen, R.A., McKenzie, D.I., Marsh, R.F.  and Aiken, J.M. (2000).  Adaptation and selection of prion protein strain conformations following interspecies transmission of transmissible mink encephalopathy.  Journal of Virology 74, 5542-5547. 

Bartz, J.C., Kincaid, A.E. and Bessen, R.A.  (2002).  Retrograde transport of transmissible mink encephalopathy within descending motor tracts. Journal of Virology 76, 5759-5768. 

Bartz, J.C., Kincaid, A.E. and Bessen, R.A.  (2003).  Rapid prion neuroinvasion following tongue infection.  Journal of Virology 77, 583-591. 

Hamir, A.N., Miller, J.M., O'Rourke, K.I., Bartz, J.C., Stack, M.J. and Chaplin, M.J. (2004).  Transmission of transmissible mink encephalopathy (TME) to raccoons (Procyon lotor) by intracerebral inoculation.  Journal of Veterinary Diagnostic Investigation 16(1), 57-63. 

Bartz, J.C., Aiken, J.M. and Bessen, R.A.  (2004).  Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy by prior peripheral inoculation with the replication deficient DY strain.  Journal of General Virology 85, 265-273. 

Mulcahey, E.M., Bartz, J.C., Kincaid, T.E. and Bessen, R.A. (2004).  Detection of PrPSc in skeletal muscle and papillae of the tongue. Journal of Virology 78, 6792-6798. 

1,2Bartz, J.C., , Crista DeJoia, C., Tucker, T., Kincaid, A.E., and Bessen,, R.A. (2005).  Extraneural prion neuroinvasion without lymphoreticular system infection.  Journal of Virology, 79, 11858-11863. 

Marsh, R.F., Kincaid, A.E., Bessen, R.A. and Bartz, J.C. (2005)   Interspecies transmission of chronic wasting disease prions to squirrel monkeys (Saimiri sciureus).  Journal of Virology, 79, 13794-13796. 

Shara, M., Yasmin, T., Kincaid, A.E., Limpach, A.L., Bartz, J.C., Brenneman, K.A., Chatterjee, A., Bagchi, M., Stohs, S.J. and Bagchi, D.(2005).  Safety and Toxicological Evaluation of a Novel Niacin-Bound Chromium (III) Complex.  Journal of Inorganic Biochemistry, 99, 2161-2183.

Hamir, A.N., Kunkle, R.A., Miller, J.M., J., Bartz, J.C. and Richt, R.A. (2006). First and Second Cattle Passage of Transmissible Mink Encephalopathy (TME) by Intracerebral Inoculation.  Veterinary Pathology, 43, 118-126.

Bartz, J.C., Kramer, M.L., Sheehan, M.H., Hutter, J.A.L., Ayers, J.I., Bessen, R.A. and Kincaid, A.E. (2007). Piron Interference is Due to a Reduction in Strain-Specific PrPSc levels. November 1st e-pub before print. Journal of Virology, 81, 689-697.

3Kincaid, A.E. and Bartz, J.C. (2007). The Nasal Cavity is a Route for Piron Infection in Hamsters. Journal of Virology, In Press

1Selected as spotlight paper by Journal of Virology, September, 2005.
2Appeared in Journal highlights of American Society of Microbiology news, November, 2005.
3This manuscript was a spotlight publication in the Journal of Virology.