Fisar 2019 Clin Biochem: Difference between revisions

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Latest revision as of 12:24, 16 September 2021

Publications in the MiPMap
FiΕ‘ar Z, JirΓ‘k R, ZvΔ›Ε™ovΓ‘ M, Setnička V, HabartovΓ‘ L, HroudovΓ‘ J, VaníčkovΓ‘ Z, Raboch J (2019) Plasma amyloid beta levels and platelet mitochondrial respiration in patients with Alzheimer's disease. Clin Biochem 72:71-80.

Β» PMID: 30954436

Fisar Zdenek, Jirak Roman, Zverova Martina, Setnicka Vladimir, Habartova Lucie, Hroudova Jana, Vanickova Zdislava, Raboch Jiri (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 AΞ²40 and AΞ²42 in patients with AD.

Plasma AΞ²40 and AΞ²42 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 AΞ²40, AΞ²42 and AΞ²42/AΞ²40 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 AΞ²42 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 AΞ² 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 AΞ² concentrations; and (3) the association between mitochondrial respiration in platelets and plasma AΞ² 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 Β© 2019. Published by Elsevier Inc. β€’ Keywords: Alzheimer's disease, Amyloid beta, Mitochondria, Plasma, Platelet β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: CZ Prague Fisar Z


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

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


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

Labels, 2019-04, MitoEAGLE blood cells data, MitoFit 2021 PLT 

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