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2015-11-26

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cc-by-nc-nd (c) Teller, Sara et al., 2015
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/101708

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

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http://dx.doi.org/10.1038/srep17261

Resum

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.

Matèries

Malaltia d'Alzheimer, Magnetita, Amiloïdosi

Matèries (anglès)

Alzheimer's disease, Magnetite, Amyloidosis

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Articles publicats en revistes (Física de la Matèria Condensada)

Citació

TELLER AMADO, Sara, et al. Magnetite-Amyloid-β deteriorates activity and functional organization in an in vitro model for Alzheimer's disease. Scientific Reports. 2015. Vol. 5, num. 17261. ISSN 2045-2322. [consulted: 27 of May of 2026]. Available at: https://hdl.handle.net/2445/101708

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