Teller Amado, SaraTahirbegi, Islam BogachanMir Llorente, MònicaSamitier i Martí, JosepSoriano i Fradera, Jordi2016-09-092016-09-092015-11-262045-2322https://hdl.handle.net/2445/101708The 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.16 p.application/pdfengcc-by-nc-nd (c) Teller, Sara et al., 2015http://creativecommons.org/licenses/by-nc-nd/3.0/esMalaltia d'AlzheimerMagnetitaAmiloïdosiAlzheimer's diseaseMagnetiteAmyloidosisinfo:eu-repo/semantics/article6555652016-09-09info:eu-repo/semantics/openAccess26608215