Reactive oxidative species enhance amyloid toxicity in APP/PS1 mouse neurons

Neurosci Bull. 2012 Jun;28(3):233-9. doi: 10.1007/s12264-012-1239-1.

Abstract

Objective: To investigate whether intracellular amyloid β (iAβ) induces toxicity in wild type (WT) and APP/PS1 mice, a mouse model of Alzheimer's disease.

Methods: Different forms of Aβ aggregates were microinjected into cultured WT or APP/PS1 mouse hippocampal neurons. TUNEL staining was performed to examine neuronal cell death. Reactive oxidative species (ROS) were measured by MitoSOXRed mitochondrial superoxide indicator.

Results: Crude, monomer and protofibril Aβ induced more toxicity in APP/PS1 neurons than in WT neurons. ROS are involved in mediating the vulnerability of APP/PS1 neurons to iAβ toxicity.

Conclusion: Oxidative stress may mediate cell death induced by iAβ in neurons.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / pathology*
  • Amyloid beta-Peptides / toxicity*
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Cell Death
  • Cells, Cultured
  • Disease Models, Animal
  • Hippocampus / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neurons / drug effects
  • Neurons / metabolism
  • Neurons / pathology*
  • Peptide Fragments / toxicity
  • Presenilin-1 / genetics
  • Reactive Oxygen Species / metabolism*

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Peptide Fragments
  • Presenilin-1
  • Reactive Oxygen Species
  • amyloid beta-protein (1-42)