The pathogenesis of neuroinvasion in Creutzfeldt-Jakob disease and other transmissible spongiform encephalopathies following the peripheral uptake of a disease agent is still not fully understood. The possibility of neuroinvasion either being established or being accelerated by an insult to the brain has not previously been tested. The experiment described herein was designed to examine this possibility by wounding the brain following an intraperitoneal challenge with a mouse-adapted strain of human transmissible spongiform encephalopathy, Fukuoka-1 strain. The results showed that brain injury introduced in any period before the appearance of cerebral abnormal prion protein deposition modified neither the clinical features, including the incubation period, nor the histopathology of the mice. Our findings suggest that neurovirulence of the agent may not be sufficiently promoted by brain injury.
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