Plasma amyloid beta levels and platelet mitochondrial respiration in patients with Alzheimer's disease

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60461373%3A22340%2F19%3A43918827" target="_blank" >RIV/60461373:22340/19:43918827 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/19:10400138 RIV/00064165:_____/19:10400138

Výsledek na webu

<a href="https://www.sciencedirect.com/science/article/pii/S0009912019303352?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0009912019303352?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.clinbiochem.2019.04.003" target="_blank" >10.1016/j.clinbiochem.2019.04.003</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Plasma amyloid beta levels and platelet mitochondrial respiration in patients with Alzheimer's disease

Popis výsledku v původním jazyce

Objectives: Altered amyloid metabolism and mitochondrial dysfunction play key roles in the development of Alzheimer&apos;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. Design and methods: 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. Results: 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. Conclusions: 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. © 2019 The Canadian Society of Clinical Chemists

Název v anglickém jazyce

Plasma amyloid beta levels and platelet mitochondrial respiration in patients with Alzheimer's disease

Popis výsledku anglicky

Objectives: Altered amyloid metabolism and mitochondrial dysfunction play key roles in the development of Alzheimer&apos;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. Design and methods: 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. Results: 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. Conclusions: 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. © 2019 The Canadian Society of Clinical Chemists

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

<a href="/cs/project/GA17-05292S" target="_blank" >GA17-05292S: Nové krevní biomarkery pro včasnou diagnostiku, prognózu a průběh Alzheimerovy nemoci</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Clinical Biochemistry

ISSN

0009-9120

e-ISSN

—

Svazek periodika

72

Číslo periodika v rámci svazku

OCT 2019

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

10

Strana od-do

71-80

Kód UT WoS článku

000486413800011

EID výsledku v databázi Scopus

2-s2.0-85063962052