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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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