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

被引：67
|
作者：
Melov, S
Wolf, N
Strozyk, D
Doctrow, SR
Bush, AI
机构：
[1] Buck Inst Age Res, Novato, CA 94945 USA
[2] Univ Washington, Dept Pathol, Seattle, WA 98195 USA
[3] Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10462 USA
[4] Eukarion, Bedford, MA 01730 USA
[5] Harvard Univ, Sch Med, Massachusetts Gen Hosp East, Lab Oxidat Biol,Genet & Aging Res Unit, Charlestown, MA 02129 USA
[6] Harvard Univ, Sch Med, Massachusetts Gen Hosp East, Dept Psychiat, Charlestown, MA 02129 USA
[7] Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia
[8] Univ Melbourne, Mental Hlth Res Inst Victoria, Parkville, Vic 3052, Australia
来源：
FREE RADICAL BIOLOGY AND MEDICINE | 2005年 / 38卷 / 02期
关键词：
free radicals;
D O I：
10.1016/j.freeradbiomed.2004.10.023
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Alzheimer disease is characterized by cerebral A 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. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码：258 / 261
页数：4
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