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Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer’s disease

The understanding of the key mechanisms behind human brain deterioration in Alzheimer’ disease (AD) is a highly active field of research. The most widespread hypothesis considers a cascade of events initiated by amyloid-β peptide fibrils that ultimately lead to the formation of the lethal amyloid pl...

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Autores principales: Teller, Sara, Tahirbegi, Islam Bogachan, Mir, Mònica, Samitier, Josep, Soriano, Jordi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4660300/
https://www.ncbi.nlm.nih.gov/pubmed/26608215
http://dx.doi.org/10.1038/srep17261
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author Teller, Sara
Tahirbegi, Islam Bogachan
Mir, Mònica
Samitier, Josep
Soriano, Jordi
author_facet Teller, Sara
Tahirbegi, Islam Bogachan
Mir, Mònica
Samitier, Josep
Soriano, Jordi
author_sort Teller, Sara
collection PubMed
description The understanding of the key mechanisms behind human brain deterioration in Alzheimer’ disease (AD) is a highly active field of research. The most widespread hypothesis considers a cascade of events initiated by amyloid-β peptide fibrils that ultimately lead to the formation of the lethal amyloid plaques. Recent studies have shown that other agents, in particular magnetite, can also play a pivotal role. To shed light on the action of magnetite and amyloid-β in the deterioration of neuronal circuits, we investigated their capacity to alter spontaneous activity patterns in cultured neuronal networks. Using a versatile experimental platform that allows the parallel monitoring of several cultures, the activity in controls was compared with the one in cultures dosed with magnetite, amyloid-β and magnetite-amyloid-β complex. A prominent degradation in spontaneous activity was observed solely when amyloid-β and magnetite acted together. Our work suggests that magnetite nanoparticles have a more prominent role in AD than previously thought, and may bring new insights in the understanding of the damaging action of magnetite-amyloid-β complex. Our experimental system also offers new interesting perspectives to explore key biochemical players in neurological disorders through a controlled, model system manner.
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spelling pubmed-46603002015-11-30 Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer’s disease Teller, Sara Tahirbegi, Islam Bogachan Mir, Mònica Samitier, Josep Soriano, Jordi Sci Rep Article The understanding of the key mechanisms behind human brain deterioration in Alzheimer’ disease (AD) is a highly active field of research. The most widespread hypothesis considers a cascade of events initiated by amyloid-β peptide fibrils that ultimately lead to the formation of the lethal amyloid plaques. Recent studies have shown that other agents, in particular magnetite, can also play a pivotal role. To shed light on the action of magnetite and amyloid-β in the deterioration of neuronal circuits, we investigated their capacity to alter spontaneous activity patterns in cultured neuronal networks. Using a versatile experimental platform that allows the parallel monitoring of several cultures, the activity in controls was compared with the one in cultures dosed with magnetite, amyloid-β and magnetite-amyloid-β complex. A prominent degradation in spontaneous activity was observed solely when amyloid-β and magnetite acted together. Our work suggests that magnetite nanoparticles have a more prominent role in AD than previously thought, and may bring new insights in the understanding of the damaging action of magnetite-amyloid-β complex. Our experimental system also offers new interesting perspectives to explore key biochemical players in neurological disorders through a controlled, model system manner. Nature Publishing Group 2015-11-26 /pmc/articles/PMC4660300/ /pubmed/26608215 http://dx.doi.org/10.1038/srep17261 Text en Copyright © 2015, Macmillan Publishers Limited 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
Teller, Sara
Tahirbegi, Islam Bogachan
Mir, Mònica
Samitier, Josep
Soriano, Jordi
Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer’s disease
title Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer’s disease
title_full Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer’s disease
title_fullStr Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer’s disease
title_full_unstemmed Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer’s disease
title_short Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer’s disease
title_sort magnetite-amyloid-β deteriorates activity and functional organization in an in vitro model for alzheimer’s disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4660300/
https://www.ncbi.nlm.nih.gov/pubmed/26608215
http://dx.doi.org/10.1038/srep17261
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