Huperzine A: is it an effective disease-modifying drug for Alzheimer's disease?

被引:75
作者
Qian, Zhong Ming [1 ]
Ke, Ya [2 ]
机构
[1] Fudan Univ, Sch Pharm, Lab Neuropharmacol, Shanghai 200433, Peoples R China
[2] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Shatin, Hong Kong, Peoples R China
基金
中国国家自然科学基金;
关键词
huperzine A; Alzheimer's disease; acetylcholinesterase inhibitor; disease-modifying agent; non-cholinergic effects; NERVE GROWTH-FACTOR; AMYLOID PRECURSOR PROTEIN; NEURONAL DEGENERATION; CHOLINESTERASE-INHIBITORS; MITOCHONDRIAL DYSFUNCTION; CORTICAL-NEURONS; NMDA RECEPTOR; BRAIN IRON; BETA; PEPTIDE;
D O I
10.3389/fnagi.2014.00216
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
Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which there is no cure. Huperzine A (HupA) is a natural inhibitor of acetylcholinesterase (AChE) derived from the Chinese folk medicine Huperzia serrata (Qian Ceng Ta). It is a licensed anti-AD drug in China and is available as a nutraceutical in the US. A growing body of evidence has demonstrated that HupA has multifaceted pharmacological effects. In addition to the symptomatic, cognitive-enhancing effect via inhibition of AChE, a number of recent studies have reported that this drug has "non-cholinergic" effects on AD. Most important among these is the protective effect of HupA on neurons against amyloid beta-induced oxidative injury and mitochondrial dysfunction as well as via the up-regulation of nerve growth factor and antagonizing N-methyl-D-aspartate receptors. The most recent discovery that HupA may reduce brain iron accumulation lends further support to the argument that HupA could serve as a potential disease-modifying agent for AD and also other neurodegenerative disorders by significantly slowing down the course of neuronal death.
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页数:6
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共 66 条
[61]   Spermidine antagonizes the inhibitory effect of huperzine A on [3H]dizocilpine (MK-801) binding in synaptic membrane of rat cerebral cortex [J].
Zhang, YH ;
Zhao, XY ;
Chen, XQ ;
Wang, Y ;
Yang, HH ;
Hu, GY .
NEUROSCIENCE LETTERS, 2002, 319 (02) :107-110
[62]   Cyclic-AMP response element binding protein and tau are involved in the neuroprotective mechanisms of nerve growth factor during focal cerebral ischemia/reperfusion in rats [J].
Zhang, Zheng-Hong ;
Xi, Gang-Ming ;
Li, Wen-Chun ;
Ling, Hai-Yan ;
Qu, Peng ;
Fang, Xiu-Bin .
JOURNAL OF CLINICAL NEUROSCIENCE, 2010, 17 (03) :353-356
[63]   Amyloid β-peptide 31-35-induced neuronal apoptosis is mediated by caspase-dependent pathways via cAMP-dependent protein kinase A activation [J].
Zhao, Li ;
Qian, Zhong-Ming ;
Zhang, Ce ;
Yung, Wing Ho ;
Fang, Du ;
Ke, Ya .
AGING CELL, 2008, 7 (01) :47-57
[64]   Activation of Group III Metabotropic Glutamate Receptor Reduces Intracellular Calcium in β-Amyloid Peptide [31-35]-Treated Cortical Neurons [J].
Zhao, Li ;
Zhao, Shen Ting ;
Qian, Zhong Ming ;
Zhang, Ce ;
Wu, Xiao Mei ;
Du, Fang ;
Ke, Ya .
NEUROTOXICITY RESEARCH, 2009, 16 (02) :174-183
[65]   2ND-GENERATION CHOLINESTERASE-INHIBITORS - EFFECT OF (L)-HUPERZINE-A ON CORTICAL BIOGENIC-AMINES [J].
ZHU, XD ;
GIACOBINI, E .
JOURNAL OF NEUROSCIENCE RESEARCH, 1995, 41 (06) :828-835
[66]   Alzheimer's disease: the two-hit hypothesis [J].
Zhu, XW ;
Raina, AK ;
Perry, G ;
Smith, MA .
LANCET NEUROLOGY, 2004, 3 (04) :219-226