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Fisar 2019 Clin Biochem

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Publications in the MiPMap
Fišar Z, Jirák R, Zvěřová M, Setnička V, Habartová L, Hroudová J, Vaníčková Z, Raboch J (2019) Plasma amyloid beta levels and platelet mitochondrial respiration in patients with Alzheimer's disease. Clin Biochem [Epub ahead of print].

» PMID: 30954436

Fisar Z, Jirak R, Zverova M, Setnicka V, Habartova L, Hroudova J, Vanickova Z, Raboch J (2019) Clin Biochem

Abstract: Altered amyloid metabolism and mitochondrial dysfunction play key roles in the development of Alzheimer's disease (AD). We asked whether an association exists between disturbed platelet mitochondrial respiration and the plasma concentrations of Aβ40 and Aβ42 in patients with AD.

Plasma Aβ40 and Aβ42 concentrations and mitochondrial respiration in intact and permeabilized platelets were measured in 50 patients with AD, 15 patients with vascular dementia and 25 control subjects. A pilot longitudinal study was performed to monitor the progression of AD in a subgroup 11 patients with AD.

The mean Aβ40, Aβ42 and Aβ42/Aβ40 levels were not significantly altered in patients with AD compared with controls. The mitochondrial respiratory rate in intact platelets was significantly reduced in patients with AD compared to controls, particularly the basal respiratory rate, maximum respiratory capacity, and respiratory reserve; however, the flux control ratio for basal respiration was increased. A correlation between the plasma Aβ42 concentration and mitochondrial respiration in both intact and permeabilized platelets differs in controls and patients with AD.

Based on our data, (1) mitochondrial respiration in intact platelets, but not the Aβ level itself, may be included in a panel of biomarkers for AD; (2) dysfunctional mitochondrial respiration in platelets is not explained by changes in plasma Aβ concentrations; and (3) the association between mitochondrial respiration in platelets and plasma Aβ levels differs in patients with AD and controls. The results supported the hypothesis that mitochondrial dysfunction is the primary factor contributing to the development of AD.

Copyright © 2019. Published by Elsevier Inc. Keywords: Alzheimer's disease, Amyloid beta, Mitochondria, Plasma, Platelet Bioblast editor: Plangger M O2k-Network Lab: CZ Prague Fisar Z


Labels: MiParea: Respiration, Patients  Pathology: Alzheimer's 

Organism: Human  Tissue;cell: Platelet  Preparation: Intact cells, Permeabilized cells 


Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, NS, ROX  HRR: Oxygraph-2k 

Labels, 2019-04