阿尔茨海默病β-淀粉样蛋白转基因小鼠会出现晶状体白内障，而抗氧化剂治疗可使其得到缓解。
Mice transgenic for Alzheimer disease beta-amyloid develop lens cataracts that are rescued by antioxidant treatment.
作者信息
Melov Simon, Wolf Norman, Strozyk Dorothea, Doctrow Susan R, Bush Ashley I
机构信息
Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA.
出版信息
Free Radic Biol Med. 2005 Jan 15;38(2):258-61. doi: 10.1016/j.freeradbiomed.2004.10.023.
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.
阿尔茨海默病的特征是大脑中β-淀粉样蛋白沉积，我们最近发现这种沉积在阿尔茨海默病患者的晶状体中也会以白内障的形式出现。在此，我们报告在阿尔茨海默病的β-淀粉样蛋白转基因小鼠模型的晶状体中，白内障显著增加，并且在用合成超氧化物歧化酶/过氧化氢酶模拟物EUK-189治疗后病情有所改善。这些数据支持与阿尔茨海默病相关的晶状体白内障的氧化病因，以及它们有被抗氧化剂预防性治疗的可能性。
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