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Neuroanatomical Distribution of Disease-Associated Prion Protein in Experimental Bovine Spongiform Encephalopathy in Cattle after Intracerebral Inoculation

Jpn. J. Infect. Dis., 65 (1), 37-44, 2012

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Shigeo Fukuda1, Sadao Onoe1, Satoshi Nikaido1, Kei Fujii1, Soichi Kageyama1, Yoshifumi Iwamaru2, Morikazu Imamura2, Kentaro Masujin2, Yuichi Matsuura2, Yoshihisa Shimizu2, Kazuo Kasai2, Miyako Yoshioka3, Yuichi Murayama2, Shirou Mohri2, Takashi Yokoyama2, and Hiroyuki Okada2*

1Animal Research Center, Hokkaido Research Organization, Hokkaido 081-0038; and 2Prion Disease Research Center and 3Pathology and Pathophysiology Research Division, National Institute of Animal Health, Ibaraki 305-0856, Japan

(Received September 2, 2011. Accepted November 17, 2011)


*Corresponding author: Mailing address: Prion Disease Research Center, National Institute of Animal Health, 3-1-5 Kan-nondai, Tsukuba, Ibaraki 305-0856, Japan. Tel: +81-29-838-8333, E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.


SUMMARY: The pathologic disease-associated prion protein (PrPSc) has been shown to be expressed in the central nervous system of Holstein cattle inoculated intracerebrally with 3 sources of classical bovine spongiform encephalopathy (BSE) isolates. Several regions of the brain and spinal cord were analyzed for PrPSc expression by immunohistochemical and Western blotting analyses. Animals euthanized at 10 months post-inoculation (mpi) showed PrPSc deposits in the brainstem and thalamus, but no vacuolation; this suggested that the BSE agent might exhibit area-dependent tropism in the brain. At 16 and 18 mpi, a small amount of vacuolation was detected in the brainstem and thalamus, but not in the cerebral cortices. At 20 to 24 mpi, when clinical symptoms were apparent, heavy PrPSc deposits were evident throughout the brain and spinal cord. The mean time to the appearance of clinical symptoms was 19.7 mpi, and the mean survival time was 22.7 mpi. These findings show that PrPSc accumulation was detected approximately 10 months before the clinical symptoms of BSE became apparent. In addition, the 3 sources of BSE prion induced no detectable differences in the clinical signs, incubation periods, neuroanatomical location of vacuoles, or distribution and pattern of PrPSc depositions in the brain.

Copyright 1998 National Institute of Infectious Diseases, Japan

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