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REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model

The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Con...

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Autores principales: Luca, Lorenzini, Alessandro, Giuliani, Sandra, Sivilia, Antonio, Baldassarro Vito, Mercedes, Fernandez, Matteo, Lotti Margotti, Luciana, Giardino, Vania, Fontani, Salvatore, Rinaldi, Laura, Calzà
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075930/
https://www.ncbi.nlm.nih.gov/pubmed/27775040
http://dx.doi.org/10.1038/srep35719
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author Luca, Lorenzini
Alessandro, Giuliani
Sandra, Sivilia
Antonio, Baldassarro Vito
Mercedes, Fernandez
Matteo, Lotti Margotti
Luciana, Giardino
Vania, Fontani
Salvatore, Rinaldi
Laura, Calzà
author_facet Luca, Lorenzini
Alessandro, Giuliani
Sandra, Sivilia
Antonio, Baldassarro Vito
Mercedes, Fernandez
Matteo, Lotti Margotti
Luciana, Giardino
Vania, Fontani
Salvatore, Rinaldi
Laura, Calzà
author_sort Luca, Lorenzini
collection PubMed
description The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Conveyer (REAC), an innovative technology platform for neuro- and bio-modulation, used according to the neuro-regenerative protocol (RGN-N), significantly increases astroglial reaction around the amyloid plaques in an AD mouse model, as evaluated by GFAP-immunoreactivity, and reduces microglia-associated neuroinflammation markers, as evaluated by Iba1-immunoreactivity and mRNA expression level of inflammatory cytokines TREM. IL1beta, iNOS and MRC1 were not affected neither by the genotype or by REAC RGN-N treatment. Also observed was an increase in locomotion in treated animals. The study was performed in 24-month-old male Tg2576 mice and age-matching wild-type animals, tested for Y-maze, contextual fear conditioning and locomotion immediately after the end of a specific REAC treatment administered for 15 hours/day for 15 days. These results demonstrated that REAC RGN-N treatment modifies pathological neuroinflammation, and mitigates part of the complex motor behaviour alterations observed in very old Tg2576 mice.
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spelling pubmed-50759302016-10-28 REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model Luca, Lorenzini Alessandro, Giuliani Sandra, Sivilia Antonio, Baldassarro Vito Mercedes, Fernandez Matteo, Lotti Margotti Luciana, Giardino Vania, Fontani Salvatore, Rinaldi Laura, Calzà Sci Rep Article The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Conveyer (REAC), an innovative technology platform for neuro- and bio-modulation, used according to the neuro-regenerative protocol (RGN-N), significantly increases astroglial reaction around the amyloid plaques in an AD mouse model, as evaluated by GFAP-immunoreactivity, and reduces microglia-associated neuroinflammation markers, as evaluated by Iba1-immunoreactivity and mRNA expression level of inflammatory cytokines TREM. IL1beta, iNOS and MRC1 were not affected neither by the genotype or by REAC RGN-N treatment. Also observed was an increase in locomotion in treated animals. The study was performed in 24-month-old male Tg2576 mice and age-matching wild-type animals, tested for Y-maze, contextual fear conditioning and locomotion immediately after the end of a specific REAC treatment administered for 15 hours/day for 15 days. These results demonstrated that REAC RGN-N treatment modifies pathological neuroinflammation, and mitigates part of the complex motor behaviour alterations observed in very old Tg2576 mice. Nature Publishing Group 2016-10-24 /pmc/articles/PMC5075930/ /pubmed/27775040 http://dx.doi.org/10.1038/srep35719 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Luca, Lorenzini
Alessandro, Giuliani
Sandra, Sivilia
Antonio, Baldassarro Vito
Mercedes, Fernandez
Matteo, Lotti Margotti
Luciana, Giardino
Vania, Fontani
Salvatore, Rinaldi
Laura, Calzà
REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model
title REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model
title_full REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model
title_fullStr REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model
title_full_unstemmed REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model
title_short REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model
title_sort reac technology modifies pathological neuroinflammation and motor behaviour in an alzheimer’s disease mouse model
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075930/
https://www.ncbi.nlm.nih.gov/pubmed/27775040
http://dx.doi.org/10.1038/srep35719
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