Neurological mechanisms of green tea polyphenols in Alzheimer's and Parkinson's diseases

被引:353
作者
Weinreb, O
Mandel, S
Amit, T
Youdim, MBH [1 ]
机构
[1] USA, Natl Parkinson Fdn, Ctr Excellence Neurodegenerat Dis Res, IL-31096 Haifa, Israel
[2] Technion Fac Med, Dept Pharmacol, Rappaport Family Res Inst, IL-31096 Haifa, Israel
关键词
green tea; (-)-epigallocatechin-3-gallate; neuroprotection; antioxidation; iron chelating; neurodegenerative diseases;
D O I
10.1016/j.jnutbio.2004.05.002
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
Tea consumption is varying its status from a mere ancient beverage and a lifestyle habit, to a nutrient endowed with possible prospective neurobiological-pharmacological actions beneficial to human health. Accumulating evidence suggest that oxidative stress resulting in reactive oxygen species generation and inflammation play a pivotal role in neurodegenerative diseases, supporting the implementation of radical scavengers, transition metal (e.g., iron and copper) chelators, and nonvitamin natural antioxidant polyphenols in the clinic. These observations are in line with the current view that polyphenolic dietary supplementation may have an impact on cognitive deficits in individuals of advanced age. As a consequence, green tea polyphenols are now being considered as therapeutic agents in well controlled epidemiological studies, aimed to alter brain aging processes and to serve as possible neuroprotective agents in progressive neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. In particular, literature on the putative novel neuroprotective mechanism of the major green tea polyphenol, (-)-epigallocatechin-3-gallate, are examined and discussed in this review. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:506 / 516
页数:11
相关论文
共 117 条
  • [1] Uptake and metabolism of epicatechin and its access to the brain after oral ingestion
    Abd El Mohsen, MM
    Kuhnle, G
    Rechner, AR
    Schroeter, H
    Rose, S
    Jenner, P
    Rice-Evans, CA
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 2002, 33 (12) : 1693 - 1702
  • [2] BATES TE, 1994, J NEUROCHEM, V63, P640
  • [3] Specific role for protein kinase Cα in the constitutive and regulated secretion of amyloid precursor protein in human skin fibroblasts
    Benussi, L
    Govoni, S
    Gasparini, L
    Binetti, G
    Trabucchi, M
    Bianchetti, A
    Racchi, M
    [J]. NEUROSCIENCE LETTERS, 1998, 240 (02) : 97 - 101
  • [4] Interleukin-1 beta and interleukin-6 are elevated in the cerebrospinal fluid of Alzheimer's and de novo Parkinson's disease patients
    BlumDegen, D
    Muller, T
    Kuhn, W
    Gerlach, M
    Przuntek, H
    Riederer, P
    [J]. NEUROSCIENCE LETTERS, 1995, 202 (1-2) : 17 - 20
  • [5] The metallobiology of Alzheimer's disease
    Bush, AI
    [J]. TRENDS IN NEUROSCIENCES, 2003, 26 (04) : 207 - 214
  • [6] BUSTO R, 1994, J NEUROCHEM, V63, P1095
  • [7] Nutritional approaches to combat oxidative stress in Alzheimer's disease
    Butterfield, DA
    Castegna, A
    Pocernich, CB
    Drake, J
    Scapagnini, G
    Calabrese, V
    [J]. JOURNAL OF NUTRITIONAL BIOCHEMISTRY, 2002, 13 (08) : 444 - 461
  • [8] TIME-COURSE OF THE TRANSLOCATION AND INHIBITION OF PROTEIN-KINASE-C DURING COMPLETE CEREBRAL-ISCHEMIA IN THE RAT
    CARDELL, M
    WIELOCH, T
    [J]. JOURNAL OF NEUROCHEMISTRY, 1993, 61 (04) : 1308 - 1314
  • [9] Parkinson's disease risks associated with cigarette smoking, alcohol consumption, and caffeine intake
    Checkoway, H
    Powers, K
    Smith-Weller, T
    Franklin, GM
    Longstreth, WT
    Swanson, PD
    [J]. AMERICAN JOURNAL OF EPIDEMIOLOGY, 2002, 155 (08) : 732 - 738
  • [10] CHECLER F, 1995, J NEUROCHEM, V65, P1431