Scrapie is a disease which occurs naturally in sheep and goats and belongs to a group of neurodegenerative disorders known as transmissible spongiform encephalopathies, or TSEs. There is currently no cure for TSEs, and the causative agent has not yet been identified. Numerous experiments, however, have addressed the pathogenetic process following a TSE infection. In this paper we present a study of the spread of the scrapie agent after intraperitoneal infection of hamsters. The accumulation of TSE-specific amyloid protein, TSE-AP (also known as PrP), was used as a marker for infectivity. The data suggested three points of agent entry into the spinal cord: the most important one between thoracic vertebrae T7-9, and two minor ones in the lower cervical spinal cord and between vertebrae T13-L2. Further, strong evidence was found for the existence of a direct route of access to the brain which bypasses the spinal cord and most likely terminates in the medulla oblongata. The indication of an alternative pathway to the brain was confirmed by the data from orally infected hamsters. The spleen appeared to play a potential, but non-essential role in pathogenesis after intraperitoneal infection in our animal model.


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