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Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer’s disease mouse model

Photobiomodulation, by utilizing low-power light in the visible and near-infrared spectra to trigger biological responses in cells and tissues, has been considered as a possible therapeutic strategy for Alzheimer’s disease (AD), while its specific mechanisms have remained elusive. Here, we demonstra...

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Autores principales: Tao, Lechan, Liu, Qi, Zhang, Fuli, Fu, Yuting, Zhu, Xi, Weng, Xiaofu, Han, Hongbin, Huang, Yong, Suo, Yuanzhen, Chen, Liang, Gao, Xiaoling, Wei, Xunbin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8423759/
https://www.ncbi.nlm.nih.gov/pubmed/34493703
http://dx.doi.org/10.1038/s41377-021-00617-3
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author Tao, Lechan
Liu, Qi
Zhang, Fuli
Fu, Yuting
Zhu, Xi
Weng, Xiaofu
Han, Hongbin
Huang, Yong
Suo, Yuanzhen
Chen, Liang
Gao, Xiaoling
Wei, Xunbin
author_facet Tao, Lechan
Liu, Qi
Zhang, Fuli
Fu, Yuting
Zhu, Xi
Weng, Xiaofu
Han, Hongbin
Huang, Yong
Suo, Yuanzhen
Chen, Liang
Gao, Xiaoling
Wei, Xunbin
author_sort Tao, Lechan
collection PubMed
description Photobiomodulation, by utilizing low-power light in the visible and near-infrared spectra to trigger biological responses in cells and tissues, has been considered as a possible therapeutic strategy for Alzheimer’s disease (AD), while its specific mechanisms have remained elusive. Here, we demonstrate that cognitive and memory impairment in an AD mouse model can be ameliorated by 1070-nm light via reducing cerebral β-amyloid (Aβ) burden, the hallmark of AD. The glial cells, including microglia and astrocytes, play important roles in Aβ clearance. Our results show that 1070-nm light pulsed at 10 Hz triggers microglia rather than astrocyte responses in AD mice. The 1070-nm light-induced microglia responses with alteration in morphology and increased colocalization with Aβ are sufficient to reduce Aβ load in AD mice. Moreover, 1070-nm light pulsed at 10 Hz can reduce perivascular microglia and promote angiogenesis to further enhance Aβ clearance. Our study confirms the important roles of microglia and cerebral vessels in the use of 1070-nm light for the treatment of AD mice and provides a framework for developing a novel therapeutic approach for AD.
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spelling pubmed-84237592021-09-14 Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer’s disease mouse model Tao, Lechan Liu, Qi Zhang, Fuli Fu, Yuting Zhu, Xi Weng, Xiaofu Han, Hongbin Huang, Yong Suo, Yuanzhen Chen, Liang Gao, Xiaoling Wei, Xunbin Light Sci Appl Article Photobiomodulation, by utilizing low-power light in the visible and near-infrared spectra to trigger biological responses in cells and tissues, has been considered as a possible therapeutic strategy for Alzheimer’s disease (AD), while its specific mechanisms have remained elusive. Here, we demonstrate that cognitive and memory impairment in an AD mouse model can be ameliorated by 1070-nm light via reducing cerebral β-amyloid (Aβ) burden, the hallmark of AD. The glial cells, including microglia and astrocytes, play important roles in Aβ clearance. Our results show that 1070-nm light pulsed at 10 Hz triggers microglia rather than astrocyte responses in AD mice. The 1070-nm light-induced microglia responses with alteration in morphology and increased colocalization with Aβ are sufficient to reduce Aβ load in AD mice. Moreover, 1070-nm light pulsed at 10 Hz can reduce perivascular microglia and promote angiogenesis to further enhance Aβ clearance. Our study confirms the important roles of microglia and cerebral vessels in the use of 1070-nm light for the treatment of AD mice and provides a framework for developing a novel therapeutic approach for AD. Nature Publishing Group UK 2021-09-08 /pmc/articles/PMC8423759/ /pubmed/34493703 http://dx.doi.org/10.1038/s41377-021-00617-3 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Tao, Lechan
Liu, Qi
Zhang, Fuli
Fu, Yuting
Zhu, Xi
Weng, Xiaofu
Han, Hongbin
Huang, Yong
Suo, Yuanzhen
Chen, Liang
Gao, Xiaoling
Wei, Xunbin
Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer’s disease mouse model
title Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer’s disease mouse model
title_full Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer’s disease mouse model
title_fullStr Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer’s disease mouse model
title_full_unstemmed Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer’s disease mouse model
title_short Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer’s disease mouse model
title_sort microglia modulation with 1070-nm light attenuates aβ burden and cognitive impairment in alzheimer’s disease mouse model
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8423759/
https://www.ncbi.nlm.nih.gov/pubmed/34493703
http://dx.doi.org/10.1038/s41377-021-00617-3
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