An assessment of the antioxidant and the antiamyloidogenic properties of melatonin: implications for Alzheimer's disease

被引:215
作者
Pappolla, MA
Chyan, YJ
Poeggeler, B
Frangione, B
Wilson, G
Ghiso, J
Reiter, RJ
机构
[1] Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78284 USA
[2] Univ S Alabama, Sch Med, Dept Pathol, Mobile, AL 36688 USA
关键词
Alzheimer's disease; amyloid beta peptide; neurofibrillary tangles; oxidative stress; free radicals; antioxidant properties of melatonin; neurodegeneration;
D O I
10.1007/s007020050018
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
This review summarizes recent advancements in our understanding of the potential role of the amyloid beta protein in Alzheimer's disease. It also discusses the significance of amyloid beta in initiating the generation of partially reduced oxygen species and points out their role in damaging essential macromolecules in the CNS which leads to neuronal dysfunction and loss. Recently acquired experimental data links these destructive oxidative processes with some neurodegenerative aspects of Alzheimer's disease. The experimental findings related to the free radical scavenging and antioxidative properties of melatonin are tabulated and its efficacy and the likely mechanisms involved in its ability to reduce neuronal damage mediated by oxygen-based reactive species in experimental models of Alzheimer's disease are summarized. Besides the direct scavenging properties and indirect antioxidant actions of melatonin, its ability to protect neurons probably also stems from its antiamyloidogenic properties. Melatonin is also unique because of the ease with which it passes through the blood-brain barrier.
引用
收藏
页码:203 / 231
页数:29
相关论文
共 216 条
  • [1] IMMUNOCHEMICAL IDENTIFICATION OF THE SERINE PROTEASE INHIBITOR ALPHA-1-ANTICHYMOTRYPSIN IN THE BRAIN AMYLOID DEPOSITS OF ALZHEIMERS-DISEASE
    ABRAHAM, CR
    SELKOE, DJ
    POTTER, H
    [J]. CELL, 1988, 52 (04) : 487 - 501
  • [2] Melatonin is protective against MPTP-induced striatal and hippocampal lesions
    AcunaCastroviejo, D
    CotoMontes, A
    Monti, MG
    Ortiz, GG
    Reiter, RJ
    [J]. LIFE SCIENCES, 1996, 60 (02) : PL23 - PL29
  • [3] Acworth I.N., 1997, OXIDANTS ANTIOXIDANT, P23
  • [4] Interaction of nascent ApoE2, ApoE3, and ApoE4 isoforms expressed in mammalian cells with amyloid peptide beta (1-40). Relevance to Alzheimer's disease
    Aleshkov, S
    Abraham, CR
    Zannis, VI
    [J]. BIOCHEMISTRY, 1997, 36 (34) : 10571 - 10580
  • [5] MELATONIN STIMULATES BRAIN GLUTATHIONE-PEROXIDASE ACTIVITY
    BARLOWWALDEN, LR
    REITER, RJ
    ABE, M
    PABLOS, M
    MENENDEZPELAEZ, A
    CHEN, LD
    POEGGELER, B
    [J]. NEUROCHEMISTRY INTERNATIONAL, 1995, 26 (05) : 497 - 502
  • [6] SOLUTION STRUCTURES OF BETA PEPTIDE AND ITS CONSTITUENT FRAGMENTS - RELATION TO AMYLOID DEPOSITION
    BARROW, CJ
    ZAGORSKI, MG
    [J]. SCIENCE, 1991, 253 (5016) : 179 - 182
  • [7] PATHOLOGICAL IMPLICATIONS OF NITRIC-OXIDE, SUPEROXIDE AND PEROXYNITRITE FORMATION
    BECKMAN, JS
    CROW, JP
    [J]. BIOCHEMICAL SOCIETY TRANSACTIONS, 1993, 21 (02) : 330 - 334
  • [8] Beckman JS, 1997, PRIMER CEREBROVASCUL, P209
  • [9] AMYLOID-BETA PEPTIDE INDUCES NECROSIS RATHER THAN APOPTOSIS
    BEHL, C
    DAVIS, JB
    KLIER, FG
    SCHUBERT, D
    [J]. BRAIN RESEARCH, 1994, 645 (1-2) : 253 - 264
  • [10] HYDROGEN-PEROXIDE MEDIATES AMYLOID-BETA PROTEIN TOXICITY
    BEHL, C
    DAVIS, JB
    LESLEY, R
    SCHUBERT, D
    [J]. CELL, 1994, 77 (06) : 817 - 827