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Acceleration of scrapie in neonatal Syrian hamsters

Department of Neurology, University of California, San Francisco, CA. (Drs. McKinley, Torchia, Mobley, and Prusiner)
Department of Anatomy, University of California, San Francisco, CA. (Dr. McKinley)
Department of Pathology, University of California, San Francisco, CA. (Dr. DeArmond)
Department of Pediatrics, University of California, San Francisco, CA. (Dr. Mobley)
Department of Neuroscience Program, University of California, San Francisco, CA. (Dr. Mobley)
Department of Biochemistry and Biophysics (Dr. Prusiner), University of California, San Francisco, CA.

Prions cause Creutzfeldt-Jakob disease, Gerstmann-Sträussler syndrome, and kuru of humans as well as scrapie of animals. Prolonged incubation periods, from months to decades, precede clinical disease. In studies on the biochemical characteristics of prions, weanling Syrian hamsters have been used extensively because they have relatively short incubation periods. In studies reported here, inoculation of neonatal hamsters significantly shortened the scrapie incubation period even further. Our results show that the scrapie incubation period in hamsters is a function of age. The interval between inoculation and death from scrapie plotted as a function of age (0 to 30 days) gave a correlation coefficient (r) of 0.86. The duration of clinical disease was also shortened in the hamsters inoculated as neonates compared with weanlings. Intraventricular injection of nerve growth factor prior to inoculation of neonates with scrapie significantly diminished the acceleration observed with scrapie alone in neonates. Histopathologic studies of brain from scrapie-inoculated neonates showed more extensive neuronal loss in the hippocampus and neocortex as well as a more profound gliosis in the caudate compared with animals inoculated as weanlings. Our results demonstrate an age-dependent acceleration of scrapie in neonatal hamsters and may provide a new experimental system for defining factors that modify the pathogenesis of prion diseases.

Address correspondence and reprint requests to Dr. McKinley, Department of Neurology, HSE-781. University of California, San Francisco, CA 94143–0518.

Supported by research grants from the National Institutes of Health (AG02132, NS14069, and NS24054), the Senator Jacob Javits Center of Excellence in Neuroscience (NS22786), and State of California, Department of Health Services (contract no. 88–94658), as well as by gifts from the Sherman Fairchild Foundation and the Armstrong McDonald Foundation, Inc.

Received March 28, 1989. Accepted for publication in final form May 2, 1989.

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