Ferroptosis and its potential role in the physiopathology of Parkinson's Disease
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F21%3A00124114" target="_blank" >RIV/00216224:14110/21:00124114 - isvavai.cz</a>
Result on the web
<a href="https://www.sciencedirect.com/science/article/pii/S0301008220301453?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0301008220301453?via%3Dihub</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.pneurobio.2020.101890" target="_blank" >10.1016/j.pneurobio.2020.101890</a>
Alternative languages
Result language
angličtina
Original language name
Ferroptosis and its potential role in the physiopathology of Parkinson's Disease
Original language description
Parkinson's Disease (PD) is a common and progressive neurodegenerative disorder characterised by motor impairments as well as non-motor symptoms. While dopamine-based therapies are effective in fighting the symptoms in the early stages of the disease, a lack of neuroprotective drugs means that the disease continues to progress. Along with the traditionally recognised pathological hallmarks of dopaminergic neuronal death and intracellular a-synuclein (alpha-syn) depositions, iron accumulation, elevated oxidative stress and lipid peroxidation damage are further conspicuous features of PD pathophysiology. However, the underlying mechanisms linking these pathological hallmarks with neurodegeneration still remain unclear. Ferroptosis, a regulated iron dependent cell death pathway involving a lethal accumulation of lipid peroxides, shares several features with PD pathophysiology. Interestingly, alpha-syn has been functionally linked with the metabolism of both iron and lipid, suggesting a possible interplay between dysregulated alpha-syn and other PD pathological hallmarks related to ferroptosis. This review will address the importance for understanding these disease mechanisms that could be targeted therapeutically. Anti-ferroptosis molecules are neuroprotective in PD animal models and the anti-ferroptotic iron chelator, deferiprone, slowed disease progression and improved motor function in two independent clinical trials for PD. An ongoing larger multi-centre phase 2 clinical trial will confirm the therapeutic potential of deferiprone and the relevance of ferroptosis in PD. This review addresses the known pathological features of PD in relation to the ferroptosis pathway with therapeutic implications of targeting this cell death pathway.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30230 - Other clinical medicine subjects
Result continuities
Project
—
Continuities
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Others
Publication year
2021
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
PROGRESS IN NEUROBIOLOGY
ISSN
0301-0082
e-ISSN
1873-5118
Volume of the periodical
196
Issue of the periodical within the volume
January 2021
Country of publishing house
GB - UNITED KINGDOM
Number of pages
12
Pages from-to
1-12
UT code for WoS article
000604785900006
EID of the result in the Scopus database
2-s2.0-85089005401