Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Abstract

A growing body of evidence suggests a relationship between oxidative stress and β-amyloid (Aβ) peptide accumulation, a hall-mark in the pathogenesis of Alzheimer's disease (AD). However, a direct causal relationship between oxidative stress and Aβ pathology has not been established in vivo. Therefore, we crossed mice with a knockout of one allele of manganese superoxide dismutase (MnSOD), a critical antioxidant enzyme, with Tg19959 mice, which overexpress a doubly mutated human β-amyloid precursor protein (APP). Partial deficiency of MnSOD, which is well established to cause elevated oxidative stress, significantly increased brain Aβ levels and Aβ plaque burden in Tg19959 mice. These results indicate that oxidative stress can promote the pathogenesis of AD and further support the feasibility of antioxidant approaches for AD therapy.

Detaljer

Författare
  • Feng Li
  • Noel Y. Calingasan
  • Fangmin Yu
  • William M. Mauck
  • Marine Toidze
  • Claudia G. Almeida
  • Reisuke H. Takahashi
  • George A. Carlson
  • M. Flint Beal
  • Michael T. Lin
  • Gunnar K. Gouras
Externa organisationer
  • Weill Cornell Medical College
  • McLaughlin Research Institute
Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Neurovetenskaper

Nyckelord

Originalspråkengelska
Sidor (från-till)1308-1312
TidskriftJournal of Neurochemistry
Volym89
Utgåva nummer5
StatusPublished - 2004 jun 1
PublikationskategoriForskning
Peer review utfördJa
Externt publiceradJa