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@ARTICLE{Kretzschmar:136879,
author = {Kretzschmar, Hans and Tatzelt, Jörg},
title = {{P}rion disease: a tale of folds and strains.},
journal = {Brain pathology},
volume = {23},
number = {3},
issn = {1015-6305},
address = {Oxford},
publisher = {Wiley-Blackwell},
reportid = {DZNE-2020-03201},
pages = {321-332},
year = {2013},
abstract = {Research on prions, the infectious agents of devastating
neurological diseases in humans and animals, has been in the
forefront of developing the concept of protein aggregation
diseases. Prion diseases are distinguished from other
neurodegenerative diseases by three peculiarities. First,
prion diseases, in addition to being sporadic or genetic
like all other neurodegenerative diseases, are infectious
diseases. Animal models were developed early on (a long time
before the advent of transgenic technology), and this has
made possible the discovery of the prion protein as the
infectious agent. Second, human prion diseases have true
equivalents in animals, such as scrapie, which has been the
subject of experimental research for many years. Variant
Creutzfeldt-Jakob disease (vCJD) is a zoonosis caused by
bovine spongiform encephalopathy (BSE) prions. Third, they
show a wide variety of phenotypes in humans and animals,
much wider than the variants of any other sporadic or
genetic neurodegenerative disease. It has now become firmly
established that particular PrP(Sc) isoforms are closely
related to specific human prion strains. The variety of
human prion diseases, still an enigma in its own right, is a
focus of this article. Recently, a series of experiments has
shown that the concept of aberrant protein folding and
templating, first developed for prions, may apply to a
variety of neurodegenerative diseases. In the wake of these
discoveries, the term prion has come to be used for Aβ,
α-synuclein, tau and possibly others. The self-propagation
of alternative conformations seems to be the common
denominator of these 'prions,' which in future, in order to
avoid confusion, may have to be specified either as
'neurodegenerative prions' or 'infectious prions.'},
subtyp = {Review Article},
keywords = {Animals / Blood-Brain Barrier / Creutzfeldt-Jakob Syndrome:
genetics / Creutzfeldt-Jakob Syndrome: pathology /
Genome-Wide Association Study / Humans / Kuru: genetics /
Kuru: pathology / PrPC Proteins: chemistry / PrPC Proteins:
genetics / PrPC Proteins: toxicity / Prion Diseases:
genetics / Prion Diseases: pathology / Prion Diseases:
transmission / Protein Folding / Proteostasis Deficiencies:
genetics / Proteostasis Deficiencies: pathology / PrPC
Proteins (NLM Chemicals)},
cin = {Ext LMU ZNP / Ext AG Tatzelt},
ddc = {610},
cid = {I:(DE-2719)5000051 / I:(DE-2719)5000053},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:23587138},
doi = {10.1111/bpa.12045},
url = {https://pub.dzne.de/record/136879},
}