After three years at NIH, Prusiner returned to UCSF to complete aresidency inneurology. Upon completion of the residency in 1974, Prusiner joined the faculty of the UCSF neurology department. Since that time, Prusiner has held various faculty and visiting faculty positions at both UCSF andUC Berkeley.[citation needed]
Since 1999, Prusiner has been director of the Institute for Neurodegenerative Diseases research laboratory at UCSF, working on prion diseases,Alzheimer's disease andtauopathies.[9]
In his 1998 PNAS review article on Prions,Prusiner wrote:[10] "The idea that scrapie prions were composed of an amyloidogenic protein was truly heretical when it was introduced" (byTikvah Alper[11][12]).Encephalopathy was a mysterious disease that attacks the brain, and leaves the brains of its victims full of holes. Scientists did not know what pathogen or disease-causing organism that produced such pattern. Prusiner and his co-workers suggested "One scientific theory, viewed as heretical in that it seems to challenge the role of nucleic acids as the exclusive carriers of genetic information." This theory suggested that this pathogen might be a "deadly variety of a normal protein that has the ability to amplify itself in the brain. The hypothetical protein is called a prion (pronounced PREE-on)."[10][13][14]
Stanley Prusiner was awarded the Nobel Prize in Physiology or Medicine in 1997 for his work in proposing an explanation for the cause ofbovine spongiform encephalopathy ("mad cow disease") and its human equivalent,Creutzfeldt–Jakob disease.[3] In this work, he coined the termprion, which comes from the words "proteinaceous" and "infectious," in 1982 to refer to a previously undescribed form of infection due to protein misfolding.[15]
^T. Alper (1966), "The exceptionally small size of the Scrapie agent",Biochemical and Biophysical Research Communications,22 (3):278–284,doi:10.1016/0006-291X(66)90478-5,PMID4957205
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