Oxidative imbalance in Alzheimer's disease

被引:120
作者
Zhu, XW [1 ]
Lee, HG
Casadesus, G
Avila, J
Drew, K
Perry, G
Smith, MA
机构
[1] Case Western Reserve Univ, Inst Pathol, Cleveland, OH 44106 USA
[2] Univ Autonoma Madrid, CSIC, Ctr Mol Biol, Fac Ciencias, E-28049 Madrid, Spain
[3] Univ Alaska, Dept Chem & Biochem, Fairbanks, AK 99701 USA
[4] Univ Alaska, Inst Arctic Biol, Fairbanks, AK 99701 USA
关键词
oxidative stress; mitochondria; metal ion; hydrogen peroxide; A beta; tau;
D O I
10.1385/MN:31:1-3:205
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Oxidative stress is a striking feature of susceptible neurons in the Alzheimer's disease brain. Importantly, because oxidative stress is an early event in Alzheimer's disease, proximal to the development of hallmark pathologies, it likely plays an important role in the pathogenesis of the disease. Investigations into the cause of such oxidative stress show that interactions between abnormal mitochondria and disturbed metal metabolism are, at least in part, responsible for cytoplasmic oxidative damage observed in these susceptible neurons, which could ultimately lead to their demise. Oxidative stress not only temporally precedes the pathological lesions of the disease but could also contribute to their formation, which, in turn, could provide some protective mechanism to reduce oxidative stress and ensure that neurons do not rapidly succumb to oxidative insults. In this review, we present the evidence for oxidative stress in Alzheimer's disease and its likely sources and consequence in relation to other pathological changes.
引用
收藏
页码:205 / 217
页数:13
相关论文
共 138 条
  • [1] The expression of key oxidative stress-handling genes in different brain regions in Alzheimer's disease
    Aksenov, MY
    Tucker, HM
    Nair, P
    Aksenova, MV
    Butterfield, DA
    Estus, S
    Markesbery, WR
    [J]. JOURNAL OF MOLECULAR NEUROSCIENCE, 1998, 11 (02) : 151 - 164
  • [2] Dramatic aggregation of Alzheimer Aβ by Cu(II) is induced by conditions representing physiological acidosis
    Atwood, CS
    Moir, RD
    Huang, XD
    Scarpa, RC
    Bacarra, NME
    Romano, DM
    Hartshorn, MK
    Tanzi, RE
    Bush, AI
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (21) : 12817 - 12826
  • [3] Static cytofluorometry and fluorescence morphology of mitochondria and DNA in proliferating fibroblasts
    Barni, S
    Sciola, L
    Spano, A
    Pippia, P
    [J]. BIOTECHNIC & HISTOCHEMISTRY, 1996, 71 (02) : 66 - 70
  • [4] HYDROGEN-PEROXIDE MEDIATES AMYLOID-BETA PROTEIN TOXICITY
    BEHL, C
    DAVIS, JB
    LESLEY, R
    SCHUBERT, D
    [J]. CELL, 1994, 77 (06) : 817 - 827
  • [5] Amyloid β-protein toxicity and oxidative stress in Alzheimer's disease
    Behl, C
    [J]. CELL AND TISSUE RESEARCH, 1997, 290 (03) : 471 - 480
  • [6] Cerebrometabolic aspects of delirium in relationship to dementia
    Blass, JP
    Gibson, GE
    [J]. DEMENTIA AND GERIATRIC COGNITIVE DISORDERS, 1999, 10 (05) : 335 - 338
  • [7] Antioxidant defences and oxidative stress markers in erythrocytes and plasma from normally nourished elderly Alzheimer patients
    Bourdel-Marchasson, I
    Delmas-Beauvieux, MC
    Peuchant, E
    Richard-Harston, S
    Decamps, A
    Reignier, B
    Emeriau, JP
    Rainfray, M
    [J]. AGE AND AGEING, 2001, 30 (03) : 235 - 241
  • [8] Cell cycle proteins in Alzheimer's disease: Plenty of wheels but no cycle
    Bowser, Robert
    Smith, Mark A.
    [J]. JOURNAL OF ALZHEIMERS DISEASE, 2002, 4 (03) : 249 - 254
  • [9] Proteomic identification of nitrated proteins in Alzheimer's disease brain
    Castegna, A
    Thongboonkerd, V
    Klein, JB
    Lynn, B
    Markesbery, WR
    Butterfield, DA
    [J]. JOURNAL OF NEUROCHEMISTRY, 2003, 85 (06) : 1394 - 1401
  • [10] Active glycation in neurofibrillary pathology of Alzheimer disease:: Nε-(carboxymethyl) lysine and hexitol-lysine
    Castellani, RJ
    Harris, PLR
    Sayre, LM
    Fujii, J
    Taniguchi, N
    Vitek, MP
    Founds, H
    Atwood, CS
    Perry, G
    Smith, MA
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 2001, 31 (02) : 175 - 180