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Jason C. Bartz, Ph.D.
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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.
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