Lack of association between cortical amyloid deposition and glucose metabolism in early stage Alzheimer ́s disease patients

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F22%3A73615824" target="_blank" >RIV/61989592:15110/22:73615824 - isvavai.cz</a>

Výsledek na webu

<a href="https://sciendo.com/article/10.2478/raon-2021-0051" target="_blank" >https://sciendo.com/article/10.2478/raon-2021-0051</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.2478/raon-2021-0051" target="_blank" >10.2478/raon-2021-0051</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Lack of association between cortical amyloid deposition and glucose metabolism in early stage Alzheimer ́s disease patients

Popis výsledku v původním jazyce

Background. Beta amyloid (Aβ) causes synaptic dysfunction leading to neuronal death. It is still controversial if the magnitude of Aβ deposition correlates with the degree of cognitive impairment. Diagnostic imaging may lead to a better understanding the role of Aβ in development of cognitive deficits. The aim of the present study was to investi-gate if Aβ deposition in the corresponding brain region of early stage Alzheimer ́s disease (AD) patients, directly cor-relates to neuronal dysfunction and cognitive impairment indicated by reduced glucose metabolism.Patients and methods. In 30 patients with a clinical phenotype of AD and amyloid positive brain imaging, 2-[18F] fluoro-2-deoxy-d-glucose (FDG) PET/CT was performed. We extracted the average [18F] flutemetamol (Vizamyl) up-take for each of the 16 regions of interest in both hemispheres and computed the standardized uptake value ratio (SUVR) by dividing the Vimazyl intensities by the mean signal of positive and negative control regions. Data were analysed using the R environment for statistical computing and graphics.Results. Any negative correlation between Aβ deposition and glucose metabolism in 32 dementia related and cor-responding brain regions in AD patients was not found. None of the correlation coefficient values were statistically significant different from zero based on two-sided p- value.Conclusions. Regional Aβ deposition did not correlate negatively with local glucose metabolism in early stage AD patients. Our findings support the role of Aβ as a valid biomarker, but does not permit to conclude that Aβ is a direct cause for an aberrant brain glucose metabolism and neuronal dysfunction.

Název v anglickém jazyce

Lack of association between cortical amyloid deposition and glucose metabolism in early stage Alzheimer ́s disease patients

Popis výsledku anglicky

Background. Beta amyloid (Aβ) causes synaptic dysfunction leading to neuronal death. It is still controversial if the magnitude of Aβ deposition correlates with the degree of cognitive impairment. Diagnostic imaging may lead to a better understanding the role of Aβ in development of cognitive deficits. The aim of the present study was to investi-gate if Aβ deposition in the corresponding brain region of early stage Alzheimer ́s disease (AD) patients, directly cor-relates to neuronal dysfunction and cognitive impairment indicated by reduced glucose metabolism.Patients and methods. In 30 patients with a clinical phenotype of AD and amyloid positive brain imaging, 2-[18F] fluoro-2-deoxy-d-glucose (FDG) PET/CT was performed. We extracted the average [18F] flutemetamol (Vizamyl) up-take for each of the 16 regions of interest in both hemispheres and computed the standardized uptake value ratio (SUVR) by dividing the Vimazyl intensities by the mean signal of positive and negative control regions. Data were analysed using the R environment for statistical computing and graphics.Results. Any negative correlation between Aβ deposition and glucose metabolism in 32 dementia related and cor-responding brain regions in AD patients was not found. None of the correlation coefficient values were statistically significant different from zero based on two-sided p- value.Conclusions. Regional Aβ deposition did not correlate negatively with local glucose metabolism in early stage AD patients. Our findings support the role of Aβ as a valid biomarker, but does not permit to conclude that Aβ is a direct cause for an aberrant brain glucose metabolism and neuronal dysfunction.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30224 - Radiology, nuclear medicine and medical imaging

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2022

Kód důvěrnosti údajů

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

Název periodika

Radiology and Oncology

ISSN

1318-2099

e-ISSN

1581-3207

Svazek periodika

56

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

SI - Slovinská republika

Počet stran výsledku

31

Strana od-do

23

Kód UT WoS článku

000734379500001

EID výsledku v databázi Scopus

2-s2.0-85122013973