Abstract
Cerebral amyloid plaques are a conspicuous pathological feature in mice infected with certain strains of scrapie. The origin of the amyloid protein in these plaques, whether locally or systemically synthesized, and the mechanisms leading to its deposition are not known. The frequency of plaques and their distribution in the brain are greatly influenced by the route of injection of the scrapie inoculum. Intracerebral (i.c.) injection consistently results in greater numbers of plaques than are obtained if the same inoculum is introduced peripherally. Following i.c. injection, plaques are commonly seen in areas close to the lateral ventricles, e.g., the corpus callosum and hippocampus; they are absent from these areas with peripheral routes. When left- and right- sided i.c. injections are compared, plaques are more frequent on the side of injection. The distribution of amyloid plaques is thus influenced either by the localization of some component of the inoculum or by traumatic damage at injection. The most plausible explanation is that amyloid deposition is associated with local concentrations of scrapie infectivity and that the amyloid protein originates in the brain.