Amyloid β-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain exists

被引:143
作者
Butterfield, D. Allan [1 ,2 ]
Griffin, Sue [3 ]
Munch, Gerald [4 ]
Pasinetti, Giulio Maria [5 ]
机构
[1] Univ Kentucky, Dept Chem, Ctr Membrane Sci, Lexington, KY 40506 USA
[2] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40506 USA
[3] VAMC, GRECC, Donald W Reynolds Dept Geriatr, Little Rock, AR 72205 USA
[4] Interdisciplinary Ctr Clin Res IZKF Leipzig, Neuroimmunol Cell Biol, D-04103 Leipzig, Germany
[5] Mt Sinai Sch Med, Dept Psychiat, Neuroinflammat Res Ctr, New York, NY 10089 USA
关键词
D O I
10.3233/JAD-2002-4309
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alzheimer's disease (AD) brain is characterized by excess deposition of amyloid beta-peptide (A beta), particularly the 42-amino acid peptide [A beta(1-42)] and by extensive oxidative stress. Several sources of the oxidative stress and inflammatory cascades are likely, including that induced by advanced glycation end products, microglial activation, and by A beta(1-42) and its sequelae. This review briefly examines each of these sources of oxidative stress and inflammation in AD brain and discusses their potential roles in the clinical progression of AD dementia.
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页码:193 / 201
页数:9
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