Mitochondrial Respiration in the Platelets of Patients with Alzheimer's Disease
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F16%3A10327724" target="_blank" >RIV/00216208:11110/16:10327724 - isvavai.cz</a>
Alternative codes found
RIV/00064165:_____/16:10327724
Result on the web
<a href="http://dx.doi.org/10.2174/1567205013666160314150856" target="_blank" >http://dx.doi.org/10.2174/1567205013666160314150856</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.2174/1567205013666160314150856" target="_blank" >10.2174/1567205013666160314150856</a>
Alternative languages
Result language
angličtina
Original language name
Mitochondrial Respiration in the Platelets of Patients with Alzheimer's Disease
Original language description
Mitochondrial dysfunctions significantly contribute to the pathogenesis of Alzheimer's disease (AD). Here, we studied the relationship between AD and changes in the mitochondrial rates of respiration in blood platelets, respiratory chain complexes activity, and coenzyme Q(10) plasma concentrations. In intact platelets obtained from AD patients, we observed a decrease in endogenous basal respiration rates, a decrease in the maximal capacity of the electron transport system (ETS), and higher respiratory rates after inhibiting complex I of the ETS. When normalized for citrate synthase activity, rotenone inhibited respiratory rates and complex I activity was significantly altered. In permeabilized platelets, mitochondrial respiration was completely rescued by the addition of complex I substrates. The changes in mitochondrial respiratory parameters were not associated with the progression of AD except for the capacity of the ETS in permeabilized platelets. In AD, complex I activity was increased, complex IV activity was decreased, and coenzyme Q(10) plasma concentrations were decreased. Our data indicate that both insufficiency in substrates entering into the oxidative phosphorylation system and functional disturbances in the ETS complex are responsible for the decrease in respiration observed in intact platelets in AD patients. Analyses of complex IV activity, the respiratory rates of intact platelets, and the capacity of the ETS in permeabilized platelets may enable the characterization of mitochondrial dysfunctions in the initial stage of AD.
Czech name
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
CE - Biochemistry
OECD FORD branch
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Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2016
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Current Alzheimer Research
ISSN
1567-2050
e-ISSN
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Volume of the periodical
13
Issue of the periodical within the volume
8
Country of publishing house
AE - UNITED ARAB EMIRATES
Number of pages
12
Pages from-to
930-941
UT code for WoS article
000380948200011
EID of the result in the Scopus database
2-s2.0-84975783236