Abstract
During transmissible spongiform encephalopathy (TSE) infections the accumulation of abnormal prion protein within the brain is often accompanied by severe neurodegeneration. Studies have implicated complement, including the membrane attack complex (MAC, C5b–C9), in inducing pathology in some neurodegenerative diseases. Recent studies show the MAC is localized on neurons in the brains of TSE patients implicating complement-mediated cell lysis in TSE neuropathology. To determine the role of the MAC in TSEs, we compared scrapie pathogenesis in C5-deficient and C5-sufficient mice. C5-deficient mice developed clinical scrapie with incubation periods similar to C5-sufficient mice. Furthermore, the severity of the neuropathology was not significantly different between C5-deficient and C5-sufficient mice. These data show that C5, and the MAC, are not involved in TSE pathogenesis.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
