The molecular basis of the prevention of Alzheimer's disease through healthy nutrition

被引:93
作者
Steele, Megan [1 ]
Stuchbury, Grant [1 ]
Munch, Gerald [1 ]
机构
[1] James Cook Univ N Queensland, Dept Biochem & Mol Biol, Comparat Genom Ctr, Townsville, Qld 4811, Australia
关键词
Alzheimer's disease; dementia; diet; antioxidant; neuroprotection; disease prevention; inflammation; oxidative stress; oxidative damage; reactive oxygen species; cytokines;
D O I
10.1016/j.exger.2006.06.002
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
The Alzheimer's disease (AD) brain shows numerous pathological phenomena, including amyloid plaques, neurofibrillary tangles, elevated levels of advanced glycation endproducts and their receptor, oxidative damage and inflammation, all of which contribute to neurodegeneration. In this review, we consider these neuropathologies associated with AD and propose that inflammation and oxidative stress play major pathogenic roles throughout disease progression. It is believed that oxidative stress and inflammation not only play major roles early in the disease, but that they act in a reinforcing cycle, amplifying their damaging effects. Therefore, epidemiological studies indicate that anti-inflammatory, antioxidant and neuroprotective agents including those from medicinal plants and health promoting foods may protect against AD, possibly through scavenging of reactive oxygen species, cytokine downregulation and strengthening the neurons antioxidant defense. This concept is further supported by evidence that certain diets (such as a Mediterranean diet) have been associated with a lower incidence of AD. This review highlights specific foods and diets thought to lower the risk of developing AD and discusses the potential of healthy nutrition in disease prevention. Published by Elsevier Inc.
引用
收藏
页码:28 / 36
页数:9
相关论文
共 75 条
  • [1] Access Economics Pty Ltd, 2004, DEL ONS ALZH DIS PRO
  • [2] Inflammation and Alzheimer's disease
    Akiyama, H
    Barger, S
    Barnum, S
    Bradt, B
    Bauer, J
    Cole, GM
    Cooper, NR
    Eikelenboom, P
    Emmerling, M
    Fiebich, BL
    Finch, CE
    Frautschy, S
    Griffin, WST
    Hampel, H
    Hull, M
    Landreth, G
    Lue, LF
    Mrak, R
    Mackenzie, IR
    McGeer, PL
    O'Banion, MK
    Pachter, J
    Pasinetti, G
    Plata-Salaman, C
    Rogers, J
    Rydel, R
    Shen, Y
    Streit, W
    Strohmeyer, R
    Tooyoma, I
    Van Muiswinkel, FL
    Veerhuis, R
    Walker, D
    Webster, S
    Wegrzyniak, B
    Wenk, G
    Wyss-Coray, T
    [J]. NEUROBIOLOGY OF AGING, 2000, 21 (03) : 383 - 421
  • [3] [Anonymous], **NON-TRADITIONAL**
  • [4] MACROPHAGE SCAVENGER RECEPTOR MEDIATES THE ENDOCYTIC UPTAKE AND DEGRADATION OF ADVANCED GLYCATION END-PRODUCTS OF THE MAILLARD REACTION
    ARAKI, N
    HIGASHI, T
    MORI, T
    SHIBAYAMA, R
    KAWABE, Y
    KODAMA, T
    TAKAHASHI, K
    SHICHIRI, M
    HORIUCHI, S
    [J]. EUROPEAN JOURNAL OF BIOCHEMISTRY, 1995, 230 (02): : 408 - 415
  • [5] Molecular mechanisms of ageing in connective tissues
    Bailey, AJ
    [J]. MECHANISMS OF AGEING AND DEVELOPMENT, 2001, 122 (07) : 735 - 755
  • [6] Mechanisms of disease - Nuclear factor-kappa b - A pivotal transcription factor in chronic inflammatory diseases
    Barnes, PJ
    Larin, M
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (15) : 1066 - 1071
  • [7] Alzheimer's disease and oxidative stress: Implications for novel therapeutic approaches
    Behl, C
    [J]. PROGRESS IN NEUROBIOLOGY, 1999, 57 (03) : 301 - 323
  • [8] Antioxidant neuroprotection in Alzheimer's disease as preventive and therapeutic approach
    Behl, C
    Moosmann, B
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 2002, 33 (02) : 182 - 191
  • [9] Braak E, 1999, EUR ARCH PSY CLIN N, V249, P14
  • [10] Bragin Valentin, 2005, Am J Alzheimers Dis Other Demen, V20, P21, DOI 10.1177/153331750502000103