BIMM 110 Lecture Notes - Lecture 3: Glycoprotein, Immunohistochemistry, Prnp
25 Feb 2017
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Carleton gajdusek: lack of inflammation categorically ruled out an infectious agent, was convinced it was genetically caused tried to. Disease agent is unknown and highly unusua. Took 4 years to set up the experiment (began in 1963) 3 chimps were incolulated with homogenized kuru brain tissue (injected directly into the brain) on sept. 17th 1963: scientists watched the 3 chimps everyday, all-day, for nearly two years with no progress. Then, in june 1965, the first symptoms of kuru were recorded: a droopy lip. Georgette was anesthetized and euthanized on oct. 28th 1965. Transmissible spongiform encephalopathies (tses): infectious hole-forming brain disease. Humans (primates: kuru, creutzfeldt-jakob disease (cjd, fatal familial insomnia (ffi, gerstmann-str ussler-scheinker syndrome (gss, mad cow disease (new variant cjd) Isolated a brain protein he named prp (prion protein) prp has two forms, normal (prpc) and abnormal (prpsc) Found that the abnormal form (prpsc) tracked with infectivity. Prions are proteins that can take on more than one 3-d structure.
