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

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.

• Authors: Simon Melov, Norman Wolf, Dorothea Strozyk, Susan R Doctrow, Ashley I Bush
• Journal: Free radical biology & medicine (Free Radic Biol Med) Vol. 38 Issue 2 Pg. 258-61 (Jan 15 2005) ISSN: 0891-5849 [Print] United States
• PMID: 15607908 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

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

Topics

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