Oxidative stress in Alzheimer's disease

被引:683
作者
Smith, MA
Rottkamp, CA
Nunomura, A
Raina, AK
Perry, G
机构
[1] Case Western Reserve Univ, Inst Pathol, Cleveland, OH 44106 USA
[2] Asahikawa Med Coll, Dept Psychiat & Neurol, Asahikawa, Hokkaido 0788510, Japan
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2000年 / 1502卷 / 01期
关键词
antioxidant; amyloid-beta; free radical; mitochondria; redox imbalance; transition metal;
D O I
10.1016/S0925-4439(00)00040-5
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
Oxidative balance is emerging as an important issue in understanding the pathogenesis of Alzheimer's disease. Examination of Alzheimer's disease brain has demonstrated a great deal of oxidative damage, associated with both hallmark pathologies (senile plaques and neurofibrillary tangles) as well as in normal appearing pyramidal neurons. While this suggests that oxidative stress is a proximal event in Alzheimer's disease pathogenesis, the mechanisms by which redox balance is altered in the disease remains elusive. Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-beta-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will. lead to a better understanding of Alzheimer's disease pathogenesis and novel therapeutic approaches. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:139 / 144
页数:6
相关论文
共 48 条
[1]   ROLE OF OXIDATIVE STRESS IN DEVELOPMENT OF COMPLICATIONS IN DIABETES [J].
BAYNES, JW .
DIABETES, 1991, 40 (04) :405-412
[2]   VITAMIN-E PROTECTS NERVE-CELLS FROM AMYLOID BETA-PROTEIN TOXICITY [J].
BEHL, C ;
DAVIS, J ;
COLE, GM ;
SCHUBERT, D .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1992, 186 (02) :944-950
[3]   HYDROGEN-PEROXIDE MEDIATES AMYLOID-BETA PROTEIN TOXICITY [J].
BEHL, C ;
DAVIS, JB ;
LESLEY, R ;
SCHUBERT, D .
CELL, 1994, 77 (06) :817-827
[4]   INDUCTION OF ALZHEIMER ANTIGENS BY AN UNCOUPLER OF OXIDATIVE-PHOSPHORYLATION [J].
BLASS, JP ;
BAKER, AC ;
KO, LW ;
BLACK, RS .
ARCHIVES OF NEUROLOGY, 1990, 47 (08) :864-869
[5]   ELECTROPHYSIOLOGICAL EFFECTS OF 25-35 AMYLOID-BETA-PROTEIN ON GUINEA-PIG LATERAL SEPTAL NEURONS [J].
CARETTE, B ;
POULAIN, P ;
DELACOURTE, A .
NEUROSCIENCE LETTERS, 1993, 151 (01) :111-114
[6]   PRODUCTION OF SUPEROXIDE ANIONS BY A CNS MACROPHAGE, THE MICROGLIA [J].
COLTON, CA ;
GILBERT, DL .
FEBS LETTERS, 1987, 223 (02) :284-288
[7]   MARKED CHANGES IN MITOCHONDRIAL-DNA DELETION LEVELS IN ALZHEIMER BRAINS [J].
CORRALDEBRINSKI, M ;
HORTON, T ;
LOTT, MT ;
SHOFFNER, JM ;
MCKEE, AC ;
BEAL, MF ;
GRAHAM, BH ;
WALLACE, DC .
GENOMICS, 1994, 23 (02) :471-476
[8]  
CRAS P, 1990, AM J PATHOL, V137, P241
[9]   RETRACTED: Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease (Retracted Article) [J].
Davis, RE ;
Miller, S ;
Herrnstadt, C ;
Ghosh, SS ;
Fahy, E ;
Shinobu, LA ;
Galasko, D ;
Thal, LJ ;
Beal, MF ;
Howell, N ;
Parker, WD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (09) :4526-4531
[10]   FREE-RADICAL DAMAGE TO PROTEINS - THE INFLUENCE OF THE RELATIVE LOCALIZATION OF RADICAL GENERATION, ANTIOXIDANTS, AND TARGET PROTEINS [J].
DEAN, RT ;
HUNT, JV ;
GRANT, AJ ;
YAMAMOTO, Y ;
NIKI, E .
FREE RADICAL BIOLOGY AND MEDICINE, 1991, 11 (02) :161-168