Mice transgenic for Alzheimer disease beta-amyloid develop lens cataracts that are rescued by antioxidant treatment

Free Radic Biol Med. 2005 Jan 15;38(2):258-61. doi: 10.1016/j.freeradbiomed.2004.10.023.

Abstract

Alzheimer disease is characterized by cerebral Abeta deposition, which we have recently discovered occurs also in the lens as cataracts in Alzheimer disease patients. Here we report the presence of significantly increased cataracts in the lenses of an Abeta-transgenic mouse model for Alzheimer disease and their amelioration upon treatment with EUK-189, a synthetic SOD/catalase mimetic. These data support an oxidative etiology for AD-associated lens cataracts and their potential to be treated preventatively with antioxidants.

Publication types

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

MeSH terms

  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / chemistry*
  • Animals
  • Antioxidants / pharmacology*
  • Catalase / pharmacology*
  • Cataract / drug therapy*
  • Cataract / metabolism*
  • Free Radicals
  • Humans
  • Mice
  • Mice, Transgenic
  • Models, Chemical
  • Organometallic Compounds / pharmacology*
  • Oxygen / chemistry
  • Salicylates / pharmacology*
  • Superoxide Dismutase / metabolism

Substances

  • Amyloid beta-Peptides
  • Antioxidants
  • EUK-189
  • Free Radicals
  • Organometallic Compounds
  • Salicylates
  • Catalase
  • Superoxide Dismutase
  • Oxygen