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Laboratory of Central Nervous System Studies (Drs. Godec and Asher, and J. Rubi, J.A. Payne, and D. Rubi-Villa), National Institute of Neurological Disorders and Stroke; the Laboratory of Neurosciences (Drs. Kozachuk, Rapoport, and Schapiro, and E. Wagner), National Institute on Aging, National Institutes of Health, Bethesda, MD; and the Department of Pathology (Dr. Masters), University of Melbourne, Parkville, Australia.
There was a report of spongiform encephalopathy transmitted to Syrian hamsters by intracerebral inoculation with the blood buffy coat of patients with Alzheimer's disease (AD) and their unaffected first-degree relatives. We attempted to verify that report, taking measures to reduce the risk of contaminating samples with agents causing spongiform encephalopathies. We obtained blood from 50 subjects, including six patients with familial AD, 21 unaffected first-degree relatives (siblings and offspring) of patients with familial AD, and 20 control subjects. We inoculated the buffy coats intracerebrally into Syrian LVG hamsters, observed them for signs of neurologic disease, examined their brains for neuropathology changes at time of death, and performed serial (blind) passages by inoculating suspensions of all recovered brains into fresh LVG hamsters. We discerned no clinical illness or histopathologic changes resembling experimental spongiform encephalopathy in any hamster inoculated with human buffy coat nor in blind-passage hamsters, nor were the life spans of those hamsters shortened. We conclude that AD is not caused by an agent that transmits spongiform encephalopathy to hamsters.
Address correspondence to Dr. David M. Asher, LCNSS, NINDS, NIH, Room 5B21, Building 36, Bethesda, MD 20892. Address reprint requests to Dr. Stanley I. Rapoport, LN, NIA, NIH, Room 6C103, Building 10, Bethesda, MD 20892.
M.S.G. was the recipient of a National Research Council Associateship
Received October 6, 1993. Accepted for publication in final form December 8, 1993.
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