Evidence of increased oxidative damage in subjects with mild cognitive impairment

被引:445
作者
Keller, JN
Schmitt, FA
Scheff, SW
Ding, Q
Chen, Q
Butterfield, DA
Markesbery, WR
机构
[1] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA
[2] Univ Kentucky, Dept Anat & Neurobiol, Lexington, KY 40536 USA
[3] Univ Kentucky, Dept Chem, Lexington, KY 40536 USA
[4] Univ Kentucky, Dept Pathol & Neurol, Lexington, KY 40536 USA
关键词
D O I
10.1212/01.WNL.0000156156.13641.BA
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective: To determine if increased levels of oxidative damage are present in the brains of persons with mild cognitive impairment (MCI), a condition that often precedes Alzheimer disease ( AD). Methods: The authors assessed the amount of protein carbonyls, thiobarbituric acid-reactive substances (TBARS), and malondialdehyde in the superior and middle temporal gyri (SMTG) and cerebellum of short postmortem interval and longitudinally evaluated normal subjects and those with MCI and early AD. Results: Elevated levels of protein carbonyls (similar to 25%), malondialdehyde (similar to 60%), and TBARS (similar to 210%) were observed in the SMTG of individuals with MCI and early AD vs normal control subjects. The elevation in TBARS was associated with the numbers of neuritic but not diffuse plaques. Levels of protein carbonyls increased as delayed verbal memory performance declined. Conclusion: Oxidative damage occurs in the brain of subjects with mild cognitive impairment, suggesting that oxidative damage may be one of the earliest events in the onset and progression of Alzheimer disease.
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收藏
页码:1152 / 1156
页数:5
相关论文
共 43 条
  • [1] [Anonymous], 1997, Neurobiol Aging, V18, pS1
  • [2] Amyloid β-protein toxicity and oxidative stress in Alzheimer's disease
    Behl, C
    [J]. CELL AND TISSUE RESEARCH, 1997, 290 (03) : 471 - 480
  • [3] NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES
    BRAAK, H
    BRAAK, E
    [J]. ACTA NEUROPATHOLOGICA, 1991, 82 (04) : 239 - 259
  • [4] Butterfield DA, 2002, NEUROBIOL AGING, V23, P655
  • [5] Amyloid β-peptide (1-42)-induced oxidative stress and neurotoxicity:: Implications for neurodegeneration in Alzheimer's disease brain.: A review
    Butterfield, DA
    [J]. FREE RADICAL RESEARCH, 2002, 36 (12) : 1307 - 1313
  • [6] CARBONNEAU MA, 1991, CLIN CHEM, V37, P1423
  • [7] OXIDATIVE STRESS, GLUTAMATE, AND NEURODEGENERATIVE DISORDERS
    COYLE, JT
    PUTTFARCKEN, P
    [J]. SCIENCE, 1993, 262 (5134) : 689 - 695
  • [8] Alzheimer neuropathologic alterations in aged cognitively normal subjects
    Davis, DG
    Schmitt, FA
    Wekstein, DR
    Markesbery, WR
    [J]. JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1999, 58 (04) : 376 - 388
  • [9] Role of the proteasome in protein oxidation and neural viability following low-level oxidative stress
    Ding, QX
    Reinacker, K
    Dimayuga, E
    Nukala, V
    Drake, J
    Butterfield, DA
    Dunn, JC
    Martin, S
    Bruce-Keller, AJ
    Keller, JN
    [J]. FEBS LETTERS, 2003, 546 (2-3): : 228 - 232
  • [10] Characterization of chronic low-level proteasome inhibition on neural homeostasis
    Ding, QX
    Dimayuga, E
    Martin, S
    Bruce-Keller, AJ
    Nukala, V
    Cuervo, AM
    Keller, JN
    [J]. JOURNAL OF NEUROCHEMISTRY, 2003, 86 (02) : 489 - 497