Can herbs provide a new generation of drugs for treating Alzheimer's disease?

被引:115
作者
Anekonda, TS [1 ]
Reddy, PH [1 ]
机构
[1] Oregon Hlth & Sci Univ, Neurogenet Lab, Neurol Sci Inst, Beaverton, OR 97006 USA
基金
美国国家卫生研究院;
关键词
Alzheimer's disease; animal model; bioavailability; herbal drug; in vitro model; mitochondria;
D O I
10.1016/j.brainresrev.2005.09.001
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The overall aim of this review is to discuss cellular mechanisms at work in the progression of AD and current therapeutic strategies for treating AD, with a focus on the potential efficacy of herbal treatments. Recent advances in molecular, cellular, and animal model studies have revealed that formation of the 4-kDa amyloid beta peptide is a key factor in the development and progression of AD. Several cellular changes have been identified that are related to amyloid beta plaques and neurofibriallary tangles found in the autopsied brains of AD patients and in AD animal models. Several therapeutic strategies have been developed to treat AD, including anti-inflammatory, anti-oxidant, and anti-amyloid approaches. Recently, herbal treatments have been tested in animal and Cellular models of AD and in clinical trials with AD subjects. In AD animal models and cell models, herbal extracts appear to have fewer adverse effects than beneficial effects on A beta and cognitive functions. These extracts have multi-functional Properties (pro-cholinergic, anti-oxidant, anti-amyloid, and anti-inflammtory), and their use in the treatment of AD patients looks promising. The chemical compositions of herbs and their potential for alleviating or reducing symptoms of AD or for affecting the disease mechanism need to be further Studied. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:361 / 376
页数:16
相关论文
共 172 条
[31]   Peripheral anti-Aβ antibody alters CNS and plasma Aβ clearance and decreases brain Aβ burden in a mouse model of Alzheimer's disease [J].
DeMattos, RB ;
Bales, KR ;
Cummins, DJ ;
Dodart, JC ;
Paul, SM ;
Holtzman, DM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (15) :8850-8855
[32]   Brain to plasma amyloid-β efflux:: a measure of brain amyloid burden in a mouse model of Alzheimer's disease [J].
DeMattos, RB ;
Bales, KR ;
Cummins, DJ ;
Paul, SM ;
Holtzman, DM .
SCIENCE, 2002, 295 (5563) :2264-2267
[33]   Phyto-oestrogens [J].
Duncan, AM ;
Phipps, WR ;
Kurzer, MS .
BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM, 2003, 17 (02) :253-271
[34]  
Eckert A, 2003, PHARMACOPSYCHIATRY, V36, pS15
[35]   Melatonin alleviates behavioral deficits associated with apoptosis and cholinergic system dysfunction in the APP 695 transgenic mouse model of Alzheimer's disease [J].
Feng, Z ;
Chang, Y ;
Cheng, Y ;
Zhang, BL ;
Qu, ZW ;
Qin, CA ;
Zhang, JT .
JOURNAL OF PINEAL RESEARCH, 2004, 37 (02) :129-136
[36]   Activity of flurbiprofen and chemically related anti-inflammatory drugs in models of Alzheimer's disease [J].
Gasparini, L ;
Ongini, E ;
Wilcock, D ;
Morgan, D .
BRAIN RESEARCH REVIEWS, 2005, 48 (02) :400-408
[37]   Non-steroidal anti-inflammatory drugs (NSAIDs) in Alzheimer's disease: old and new mechanisms of action [J].
Gasparini, L ;
Ongini, E ;
Wenk, G .
JOURNAL OF NEUROCHEMISTRY, 2004, 91 (03) :521-536
[38]   Immunotherapy for Alzheimer's disease [J].
Gelinas, DS ;
DaSilva, K ;
Fenili, D ;
George-Hyslop, PS ;
McLaurin, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 :14657-14662
[39]   Curcumin, the active constituent of turmeric, inhibits amyloid peptide-induced cytochemokine gene expression and CCR5-mediated chemotaxis of THP-1 monocytes by modulating early growth response-1 transcription factor [J].
Giri, RK ;
Rajagopal, V ;
Kalra, VK .
JOURNAL OF NEUROCHEMISTRY, 2004, 91 (05) :1199-1210
[40]   Billion-dollar market blossoms as botanicals take root [J].
Glaser, V .
NATURE BIOTECHNOLOGY, 1999, 17 (01) :17-18