Additive Impairment of Synaptic Signaling in Cultured Cortical Neurons by Exogenously-Applied Oligomerized Amyloid-β and Airborne Nanoparticles Generated during Photocopying
Affiliations: [a] Laboratory for Neuroscience, University of Massachusetts Lowell, Lowell, MA, USA | [b] Nanomanufacturing Center for Excellence, University of Massachusetts Lowell, Lowell, MA, USA | [c] Departments of Biological Sciences, University of Massachusetts Lowell, Lowell, MA, USA | [d] Departments of Work Environment, University of Massachusetts Lowell, Lowell, MA, USA | [e] Biomedical Engineering and Biotechnology Program, University of Massachusetts Lowell, Lowell, MA, USA
Correspondence:
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Correspondence to: Thomas B. Shea, University of Massachusetts Lowell, 1 University Avenue, Lowell, MA 01821, USA, Tel.: +1 978 934 2881; Fax: +1 978 934 3044; thomas_shea@uml.edu
Abstract: Photocopying in offices and printing centers releases nanoparticles that can reach the brain following inhalation. We examined whether subcytotoxic levels of airborne photocopy-emitted nanoparticles could potentiate perturbation of synaptic signaling in cultured neurons following exposure to amyloid-β (Aβ). Signaling was only transiently inhibited by Aβ or nanoparticles individually, but remained statistically reduced in cultures receiving both after 24 h. In vitro and in vivo studies with copier emitted nanoparticles have consistently demonstrated inflammation, oxidative stress, and cytotoxicity. Since Aβ can accumulate years before cognitive decline, subcytotoxic levels of nanoparticles are one factor that could potentiate Aβ-induced impairment of synaptic activity during these early stages.
