Judd M. Aiken, PhD

Professor Animal Health and Biomedical Sciences School of Veterinary Medicine University of Wisconsin 1656 Linden Drive Madison, WI 53706-1581 Phone: 608-262-3177 Fax: 608-262-7420 Email: aiken@svm.vetmed.wisc.edu Web: http://www.ahabs.wisc.edu/~aikenlab

Research Areas

Virology

Research Description

We have two major projects in my laboratory: i) the involvement of mitochondria in the aging process and ii) the molecular characterization of the scrapie agent. We are testing the hypothesis that mitochondrial DNA is a "weak link" in the aging process. We are examining two animal species, the mouse and the rhesus monkey for the presence of age-associated mtDNA abnormalities. We have identified age-associated mtDNA deletions in both species. These age-associated deletions appear to be most pronounced in nerve and muscle and hold great promise for explaining the major diseases and disorders old age brings to these tissues. Our current efforts involve quantification of deletion abundance and correlation of deletions with changes in cellular morphology. Transmissible spongiform encephalopathies (TSEs) are fatal neurologic disorders that are characterized by extended incubation periods, of months to years, followed by rapid progression of clinical symptoms. TSEs affect a wide range of animal hosts with scrapie, in sheep and goats, being the most common natural TSE. Human forms of TSE include Gerstmann-Straussler-Scheinker syndrome (GSS), Creutzfeldt-Jakob disease (CJD) and kuru. The causative agent of TSEs remains elusive with hypotheses ranging from the agent being a virus to self-replicating protein hypothesis (prion hypothesis). My laboratory is using molecular methodologies to identify the etiologic agent. We have, in addition, recently developed an in vitro system for the identification of drugs having therapeutic benefit.

Publications

• Iniguez, V., McKenzie, D., Mirwald, J. and Aiken, J.M . (2000). Strain-specific propagation of PrPSc properties into baculovirus expressed PrPC. J. Gen. Virol. 81: 2565-2571. Abstract, Full Text (PDF)
• Bartz, J.C., R.A. Bessen, R.F. Marsh, D. McKenzie and J.M. Aiken. 2000. Emergence and competition of prion protein strain conformations following interspecies TSE transmission. J. Virol. 74: 5542-5547.
• Wanagat, J., Cao,Z., Pathare, P. and Aiken, J.M.. (2001). Mitochondrial DNA deletion mutations co-localize with segmental electron transport system abnormalities, muscle fiber atrophy, fiber splitting and oxidative damage in sarcopenia. FASEB J. 15: 322-332. Abstract, Full Text (PDF)
• Bua, E., J. Wanagat and J.M. Aiken. 2001. Mitochondrial DNA abnormalities. In The Encyclopedia of Aging, Ed. by G.L. Maddox. Springer Publishing Co. 696-697.
• Wanagat, J., M.E. Lopez and J.M. Aiken. 2001. Mitochondrial DNA alterations. In Handbook of the Biology of Aging, Ed. by E.J. Masoro and S.N. Austad. Academic Press, 114-139.
• Cao, Z., J. Wanagat, S. McKiernan and J.M. Aiken. 2001. Mitochondrial DNA deletions are concomitant with ragged red regions of individual, aged muscle fibers: analysis by laser capture dissection. Nucleic Acids. Res. 29: 4502-4508.
• Wanagat, J., M.R. Wolff and J.M. Aiken. 2002. Age-associated changes in function, structure and mitochondrial genetic and enzymatic abnormalities in the Fischer 344 x Brown Norway F1 hybrid rat heart. J. Mol. Cell. Cardiol. 34:17-28.
• Bua, E., S. McKiernan, J. Wanagat, D. McKenzie and J.M. Aiken. 2002. Mitochondrial abnormalities accumulate in muscles that undergo sarcopenia. J. Applied Physiol. 92: 2617-2624.
• Aiken, J., E. Bua, Z. Cao, M. Lopez, J. Wanagat, D. McKenzie and S. McKiernan. 2002. Mitochondrial DNA deletion mutations and sarcopenia. N.Y. Acad. Sci. 959: 412-423.
• McKenzie, D., E. Bua, S. McKiernan, Z. Cao, J. Wanagat and J.M. Aiken. 2002. Mitochondrial DNA deletion mutations: a causal role in sarcopenia. Eur. J. Biochem. 269: 2010-2015.
• Pak, J.W., A. Herbst, E. Bua, N. Gokey, D. McKenzie and J.M. Aiken. Mitochondrial DNA mutations as a fundamental mechanism in physiological declines associated with aging. Aging Cell 2: 1-7.
• Pak, J.W., A. Herbst, E. Bua, N. Gokey, D. McKenzie and J.M. Aiken. 2003. Mitochondrial theory of aging: alive and well. Aging Cell 2: 8-10.
• Cao, Z., R.L. Tanguay, D. McKenzie, R.E. Peterson and J.M. Aiken. 2003. Identification of 2,3,7,8-Tetrachlorodibenzo- p-dioxin-response calcium binding protein genes in zebrafish (Danio rerio) and rainbow trout (Oncorhynchus mykiss). Aquatic Toxicology 63:271-282.
• Johnson, C.J., J. Johnson, M. Clayton, D. McKenzie and J.M. Aiken. 2003. PrP gene heterogeneity in deer from the CWD-endemic region of Wisconsin. J. Wildlife Dis., 39:576- 581.
• Bartz, J.C., J.M. Aiken and R.A. Bessen. Extension of transmissible mink encephalopathy incubation period by superinfection with a replication-deficient prion strain. J. Gen. Virol., in press.
• McKiernan, S.M., Bua, E., McGorray, J. and J.M. Aiken. 2004. Early-onset calorie restriction conserves fiber number in aging rat skeletal muscle. FASEB Journal Express Article 10.1096/fj.03-0667fje.
• Bua, E., McKiernan, S.M. and J.M. Aiken. 2004. Caloric restriction affects onset but not accumulation of ETS abnormalities in rat skeletal muscle. FASEB Journal Express Article 10.1096/fj.03-0668fje.
• Bartz, J.C., J.M. Aiken and R.A. Bessen. 2004. Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain. J. Gen. Virol. 85265-85273.
• Bartz, J.C., J.M. Aiken and R.A. Bessen. Extension of transmissible mink encephalopathy incubation period by superinfection with a replication-deficient prion strain. J. Gen. Virol., in press.

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