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@ARTICLE{Tamgney:140025,
author = {Tamgüney, Gültekin and Korczyn, Amos D},
title = {{A} critical review of the prion hypothesis of human
synucleinopathies.},
journal = {Cell $\&$ tissue research},
volume = {373},
number = {1},
issn = {0302-766X},
address = {Heidelberg},
publisher = {Springer},
reportid = {DZNE-2020-06347},
pages = {213-220},
year = {2018},
abstract = {Parkinson's disease (PD), dementia with Lewy bodies (DLB),
and multiple system atrophy (MSA) are neurodegenerative
disorders which have been pathologically classified as
synucleinopathies, since they are associated with
pathognomonic deposits of misfolded alpha-synuclein in cells
of the nervous system. Recently PD, DLB, and MSA were also
suggested to be prion-like disorders. Much controversy
exists regarding this analogy between synucleinopathies and
prion diseases. Here, we discuss what characterizes prion
diseases and in which way synucleinopathies may be
considered prion-like or -unlike. We critically review
recent clinical and in vivo evidence from transmission
studies to animals in support of or questioning the prion
hypothesis of human synucleinopathies. We conclude that,
although PD, DLB, and MSA fulfill many criteria of
prion-likeness, they also still fail some of these
criteria.},
subtyp = {Review Article},
keywords = {Humans / Models, Biological / Neurodegenerative Diseases:
metabolism / Neurodegenerative Diseases: pathology / Prions:
metabolism / alpha-Synuclein: metabolism / Prions (NLM
Chemicals) / alpha-Synuclein (NLM Chemicals)},
cin = {AG Tamgüney 2},
ddc = {610},
cid = {I:(DE-2719)1013022},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:29116402},
doi = {10.1007/s00441-017-2712-y},
url = {https://pub.dzne.de/record/140025},
}