title: Reactive oxidative species enhance amyloid toxicity in APP/PS1 mouse neurons.
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.
  
  
  CONCLUSIONS
  Oxidative stress may mediate cell death induced by iAβ in neurons.
authors.affiliation: State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Yang
authors.forename: Xiaqin
authors.initials: X
authors.lastname: Sun
authors.forename: Hilal
authors.initials: H
authors.lastname: Lashuel
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000633:toxicity*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D016923:Cell Death; D002478:Cells, Cultured; D004195:Disease Models, Animal; D006624:Hippocampus / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D010446:Peptide Fragments / Q000633:toxicity; D053764:Presenilin-1 / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D010446:Peptide Fragments; D053764:Presenilin-1; D017382:Reactive Oxygen Species; C075222:amyloid beta-protein (1-42)