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

Result code in 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>

Alternative codes found

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

Result on the web

<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>

Result language

angličtina

Original language name

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

Original language description

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

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30103 - Neurosciences (including psychophysiology)

Project

<a href="/en/project/GA17-05292S" target="_blank" >GA17-05292S: Novel blood-based biomarkers for early diagnosis, prognosis and progress of Alzheimer's disease</a><br>

Continuities

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

Publication year

2019

Confidentiality

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

Name of the periodical

Clinical Biochemistry

ISSN

0009-9120

e-ISSN

—

Volume of the periodical

72

Issue of the periodical within the volume

OCT 2019

Country of publishing house

GB - UNITED KINGDOM

Number of pages

10

Pages from-to

71-80

UT code for WoS article

000486413800011

EID of the result in the Scopus database

2-s2.0-85063962052