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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

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    CE - Biochemistry

  • OECD FORD branch

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

  • 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