Additive Impairment of Synaptic Signaling in Cultured Cortical Neurons by Exogenously-Applied Oligomerized Amyloid-β and Airborne Nanoparticles Generated during Photocopying

J Alzheimers Dis. 2015;47(1):49-54. doi: 10.3233/JAD-150099.

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.

Keywords: Amyloid-β; multi-electrode arrays; nanoparticles; neurotoxicology; signaling.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials / drug effects
  • Amyloid beta-Peptides / pharmacology*
  • Analysis of Variance
  • Animals
  • Cells, Cultured
  • Cerebral Cortex / cytology*
  • Copying Processes*
  • Dose-Response Relationship, Drug
  • Embryo, Mammalian
  • Female
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Nanoparticles / toxicity*
  • Neurons / drug effects*
  • Peptide Fragments / pharmacology*
  • Pregnancy
  • Signal Transduction / drug effects
  • Synapses / drug effects*

Substances

  • Amyloid beta-Peptides
  • Peptide Fragments
  • amyloid beta-protein (1-42)