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Sci Rep. 2015 Nov 26;5:17261. doi: 10.1038/srep17261.

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

Author information

1
Departament d'Estructura i Constituents de la Matèria, Universitat de Barcelona, Barcelona, E-08028, Spain.
2
Nanobioengineering Group, Institute for Bioengineering of Catalonia (IBEC), Barcelona, E-08028, Spain.
3
Departament d'Electrònica, Universitat de Barcelona, Barcelona, E-08028, Spain.
4
Centro de Investigación Biomédica en Red en Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), Barcelona, E-08028, Spain.

Abstract

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.

PMID:
26608215
PMCID:
PMC4660300
DOI:
10.1038/srep17261
[Indexed for MEDLINE]
Free PMC Article

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