RESUMO
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-ß (Aß). Signaling was only transiently inhibited by Aß or nanoparticles individually, but remained statistically reduced in cultures receiving both after 24âh. In vitro and in vivo studies with copier emitted nanoparticles have consistently demonstrated inflammation, oxidative stress, and cytotoxicity. Since Aß can accumulate years before cognitive decline, subcytotoxic levels of nanoparticles are one factor that could potentiate Aß-induced impairment of synaptic activity during these early stages.