Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice

Anton Malkov, Irina Popova et al. demonstrate that beta-amyloid application induces oxidative stress and reduces glucose consumption in the mouse brain, leading to network hyperactivity and behavioral changes—pathologies similar to those observed early on in Alzheimer’s disease patients. Inhibition...

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Main Authors:	Anton Malkov, Irina Popova, Anton Ivanov, Sung-Soo Jang, Seo Yeon Yoon, Alexander Osypov, Yadong Huang, Yuri Zilberter, Misha Zilberter
Format:	Article
Language:	English
Published:	Nature Publishing Group 2021-09-01
Series:	Communications Biology
Online Access:	https://doi.org/10.1038/s42003-021-02551-x

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spelling	doaj-a6c2412d4513481a8cfa406b0388ad5a2021-09-12T11:12:09ZengNature Publishing GroupCommunications Biology2399-36422021-09-014111210.1038/s42003-021-02551-xAβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in miceAnton Malkov0Irina Popova1Anton Ivanov2Sung-Soo Jang3Seo Yeon Yoon4Alexander Osypov5Yadong Huang6Yuri Zilberter7Misha Zilberter8Institute of Theoretical and Experimental Biophysics, Russian Academy of SciencesInstitute of Theoretical and Experimental Biophysics, Russian Academy of SciencesAix Marseille Université, InsermGladstone Institute of Neurological DiseaseGladstone Institute of Neurological DiseaseInstitute of Theoretical and Experimental Biophysics, Russian Academy of SciencesGladstone Institute of Neurological DiseaseAix Marseille Université, InsermGladstone Institute of Neurological DiseaseAnton Malkov, Irina Popova et al. demonstrate that beta-amyloid application induces oxidative stress and reduces glucose consumption in the mouse brain, leading to network hyperactivity and behavioral changes—pathologies similar to those observed early on in Alzheimer’s disease patients. Inhibition of NADPH oxidase 2 (NOX2) rescued these phenotypes, suggesting that NOX2 may represent an important therapeutic target for Alzheimer’s disease.https://doi.org/10.1038/s42003-021-02551-x
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Anton Malkov Irina Popova Anton Ivanov Sung-Soo Jang Seo Yeon Yoon Alexander Osypov Yadong Huang Yuri Zilberter Misha Zilberter
spellingShingle	Anton Malkov Irina Popova Anton Ivanov Sung-Soo Jang Seo Yeon Yoon Alexander Osypov Yadong Huang Yuri Zilberter Misha Zilberter Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice Communications Biology
author_facet	Anton Malkov Irina Popova Anton Ivanov Sung-Soo Jang Seo Yeon Yoon Alexander Osypov Yadong Huang Yuri Zilberter Misha Zilberter
author_sort	Anton Malkov
title	Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice
title_short	Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice
title_full	Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice
title_fullStr	Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice
title_full_unstemmed	Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice
title_sort	aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via nox2-induced oxidative stress in mice
publisher	Nature Publishing Group
series	Communications Biology
issn	2399-3642
publishDate	2021-09-01
description	Anton Malkov, Irina Popova et al. demonstrate that beta-amyloid application induces oxidative stress and reduces glucose consumption in the mouse brain, leading to network hyperactivity and behavioral changes—pathologies similar to those observed early on in Alzheimer’s disease patients. Inhibition of NADPH oxidase 2 (NOX2) rescued these phenotypes, suggesting that NOX2 may represent an important therapeutic target for Alzheimer’s disease.
url	https://doi.org/10.1038/s42003-021-02551-x
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Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice

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