Mitochondrial Respiration in the Platelets of Patients with Alzheimer's Disease
Language English Country United Arab Emirates Media print
Document type Journal Article
PubMed
26971932
DOI
10.2174/1567205013666160314150856
PII: CAR-EPUB-74360
Knihovny.cz E-resources
- MeSH
- Alzheimer Disease genetics metabolism MeSH
- Apolipoproteins E genetics MeSH
- Biomarkers metabolism MeSH
- Citrate (si)-Synthase metabolism MeSH
- Gene Frequency MeSH
- Middle Aged MeSH
- Humans MeSH
- Mitochondria metabolism MeSH
- Polymorphism, Genetic MeSH
- Electron Transport Complex I metabolism MeSH
- Electron Transport Complex IV metabolism MeSH
- ROC Curve MeSH
- Aged MeSH
- Blood Platelets metabolism MeSH
- Ubiquinone analogs & derivatives blood MeSH
- Mental Status Schedule MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Apolipoproteins E MeSH
- Biomarkers MeSH
- Citrate (si)-Synthase MeSH
- coenzyme Q10 MeSH Browser
- Electron Transport Complex I MeSH
- Electron Transport Complex IV MeSH
- Ubiquinone MeSH
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 Q10 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 Q10 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.
References provided by Crossref.org
CoQ10 and Mitochondrial Dysfunction in Alzheimer's Disease
Coenzyme Q10: A Biomarker in the Differential Diagnosis of Parkinsonian Syndromes
Age-Dependent Alterations in Platelet Mitochondrial Respiration
Impact of aging on mitochondrial respiration in various organs
Mitochondrial respiration of human platelets in young adult and advanced age - Seahorse or O2k?
In vitro effects of antipsychotics on mitochondrial respiration