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NEUROLOGY 1996;46:532-537
© 1996 American Academy of Neurology

Experimental transmission of Creutzfeldt-Jakob disease and related diseases to rodents

J. Tateishi, MD, T. Kitamoto, MD, M. Z. Hoque, MD and H. Furukawa, MD

From the Department of Neuropathology, Neurological Institute, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Supported by grants from the Science and Technology Agency, Japan, and the Ministry of Education, Science and Culture, Japan.
Received December 12, 1994. Accepted in final form April 20, 1995.
Address correspondence and reprint requests to Dr. Jun Tateishi, Department of Neuropathology, Neurological Institute, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashiku, Fukuoka 812, Japan.

Sporadic Creutzfeldt-Jakob disease (CJD) with 129M/M, and iatrogenic and familial CJD with E200K and M232R, showed similar clinicopathologic features, a synaptic type deposition of PrPCJD, and high transmission frequencies to mice. Sporadic patients with 129M/V or 129V/V, and mutation cases with V180I, showed slightly different features and low or null transmission frequencies to mice. Hereditary cases with P102L, P105L, A117V, Y145stop, and insertions had different features but all demonstrated a long clinical duration and the presence of PrP plaques. The experimental transmission to mice of these mutant forms was difficult, except for one-third of the cases with P102L. CJD and related diseases, even those that are hereditary, may thus be divided into two different groups, those that are easily transmissible and those that are either difficult to transmit or nontransmissible.

NEUROLOGY 1996,46 532-537




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