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@ARTICLE{Outeiro:282333,
author = {Outeiro, Tiago Fleming and Höglinger, Günter and Lang,
Anthony E and Vieira, Tuane C R G},
title = {{P}rotein misfolding: understanding biology to classify and
treat synucleinopathies.},
journal = {Journal of neural transmission},
volume = {132},
number = {11},
issn = {0375-9245},
address = {Wien [u.a.]},
publisher = {Springer},
reportid = {DZNE-2025-01294},
pages = {1645 - 1654},
year = {2025},
abstract = {Protein misfolding and aggregation is a major pathological
hallmark in a variety of human conditions, including cancer,
diabetes, and neurodegeneration. However, we still do not
fully understand the role of protein accumulation in
disease. Interestingly, recent breakthroughs in artificial
intelligence (AI) are having a tremendous impact on our
ability to predict three-dimensional protein structures and
understand the molecular rules governing protein
folding/misfolding. This progress will enable us to
understand how intrinsic and extrinsic factors trigger
protein misfolding, thereby changing protein function. These
changes, in some cases, are related to normal biological
responses and, in other cases, associated with pathological
alterations, such as those found in many neurodegenerative
disorders. Here, we provide a brief historical perspective
of how findings in the field of prion diseases and prion
biology have enabled tremendous advances that are now
forming the basis for our understanding of disease processes
and discuss how this knowledge is now emerging as central
for our ability to classify, diagnose, and treat devastating
neurodegenerative disorders such as Parkinson's and
Alzheimer's diseases.},
subtyp = {Review Article},
keywords = {Humans / Synucleinopathies: metabolism / Synucleinopathies:
classification / Synucleinopathies: therapy / Protein
Folding / Proteostasis Deficiencies: metabolism /
Proteostasis Deficiencies: therapy / Animals /
Alpha-synuclein (Other) / Biomarkers (Other) / Disease
classification (Other) / Neurodegeneration (Other) /
Parkinson’s disease (Other) / Protein aggregation (Other)},
cin = {AG Fischer / Clinical Research (Munich)},
ddc = {610},
cid = {I:(DE-2719)1410002 / I:(DE-2719)1111015},
pnm = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39932548},
doi = {10.1007/s00702-025-02889-0},
url = {https://pub.dzne.de/record/282333},
}