ABSTRACT: "While host PrP is essential for TSE agent spread and replication, excessive production of all forms of PrP can be inappropriately perpetuated by living cells, even after the initiating infectious agent is eliminated. Host PrP (amyloid) changes can start as a protective innate immune response that ultimately escapes control. A subset of other neurodegenerative and amyloid diseases, including non-transmissible AD, may be initiated by environmental infectious agents that are no longer present."
Kohtaro Miyazawa, Terry Kipkorir, Sarah Tittman, Laura Manuelidis
PlosOne, Received February 10, 2012; Accepted March 17, 2012; Published April 11, 2012