Journal
SCIENTIFIC REPORTS
Volume 5, Issue -, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/srep17261
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Funding
- Ministerio de Ciencia e Innovacion (Spain) [FIS2011-28820-C02-01, FIS2013-41144-P]
- Generalitat de Catalunya [2009-SGR-14, 2014-SGR-878]
- VI National RDi Plan
- Iniciativa Ingenio 2010
- Consolider Program
- Instituto de Salud Carlos III
- Commission for Universities and Research of Department of Innovation, Universities
- Enterprise of the Generalitat de Catalunya [2014-SGR-1442]
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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-beta 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-beta 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-beta and magnetite-amyloid-beta complex. A prominent degradation in spontaneous activity was observed solely when amyloid-beta 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-beta 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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