Malondialdehyde Mediated Alpha-Synuclein Aggregation: A Plausible Etiology of Parkinson's Disease in Oxidative Stress
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F25%3A00082439" target="_blank" >RIV/00159816:_____/25:00082439 - isvavai.cz</a>
Alternative codes found
RIV/00216224:14110/25:00143786
Result on the web
<a href="https://pubs.acs.org/doi/10.1021/acs.chemrestox.4c00348" target="_blank" >https://pubs.acs.org/doi/10.1021/acs.chemrestox.4c00348</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1021/acs.chemrestox.4c00348" target="_blank" >10.1021/acs.chemrestox.4c00348</a>
Alternative languages
Result language
angličtina
Original language name
Malondialdehyde Mediated Alpha-Synuclein Aggregation: A Plausible Etiology of Parkinson's Disease in Oxidative Stress
Original language description
Malondialdehyde (MDA), a major reactive byproduct of lipid peroxidation, has been implicated in numerous pathological conditions as a result of altering the structure and function of crucial proteins. One such protein is alpha-synuclein (alpha-Syn), which plays a vital role in the pathogenesis of Parkinson's disease (PD). This study investigates the hypothesis that MDA causes structural alterations in alpha-Syn, promoting its aggregation and exacerbating its toxicological effects. In vivo experiments were conducted where MDA and MDA-modified alpha-Syn were injected to the brain of mice. Behavioral assessments were performed to evaluate motor function changes, while immunohistochemistry was employed to examine the extent of alpha-Syn aggregation in brain tissues. An extraction protocol was also developed exquisitely, enabling quantification of modified alpha-Syn from brain tissue. Moreover, 15Nitrogen-labeled alpha-Syn was employed to establish an absolute quantification method on nLC-HRMS/MS. Our findings demonstrate that MDA-induced modifications in alpha-Syn alter its structural properties and also significantly enhance its aggregation propensity, potentially contributing to the neurodegenerative processes observed in PD. The developed model displayed a nonreversible decline in motor function, neurodegeneration, and aggregation of proteins in the brain mimicking the PD conditions. This research provides valuable insights into the molecular mechanisms of PD, emphasizing the role of MDA-modified proteins in the etiology of PD.
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
30105 - Physiology (including cytology)
Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
CHEMICAL RESEARCH IN TOXICOLOGY
ISSN
0893-228X
e-ISSN
1520-5010
Volume of the periodical
38
Issue of the periodical within the volume
4
Country of publishing house
US - UNITED STATES
Number of pages
10
Pages from-to
573-582
UT code for WoS article
001461031900001
EID of the result in the Scopus database
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