Hi Edward,
thanks for posting the complete study!
I found the following findings especially interesting:
"Huperzine A (HupA), a novel Lycopodium alkaloid isolated from Chinese folk
medicine Huperzia serrata (Qian Ceng Ta), is a potent, selective, and well-tolerated
inhibitor of AChE. A large number of studies have shown that HupA has mild-tono
side effects or toxicity in mice, rats, rabbits and dogs, without fasciculation or
other cholinergic hyperactivity symptoms, and shows no histopathological changes
after subacute administration (reviewed by (Wang et al. 2006a))."
"A large number of clinical studies have
shown that HupA administration can significantly improve the memory, cognitive
skills, and daily life abilities of AD patients while showing no severe side effects.
HupA can also markedly improve the memory impairment in vascular dementia
(VD) patients. In addition, HupA was reported to ameliorate the memory deficits in
schizophrenia patients and improve sleep in insomniacs."
"Recent data indicate that HupA has multiple neuroprotective effects aside from its
AChE inhibition, which include regulating b-amyloid precursor protein (APP)
metabolism and counteracting Ab-associated neurotoxicity. This may provide adequate
evidence for the clinical and experimental improvement gained from HupA
(reviewed by (Zhang and Tang 2006)). In the present paper, the classic AChE
inhibitory effect of HupA and its new neuroprotective targets on AD pathology will
be reviewed."
"HupA is a mixed-competitive and reversible AChE inhibitor, which shows higher
potency and selectivity of AChE inhibition both in vitro and in vivo as compared with
galanthamine, donepezil, tacrine, and rivastigmine (reviewed by (Wang et al. 2006a)).
Our recent study also showed that HupA has an 8- and 2-fold higher potency for
increasing cortical ACh level than donepezil and rivastigmine, respectively, with a
longer duration of action and fewer side effects (Liang and Tang 2004)."
"Neuroprotective Effects of HupA on APP Processing"
"Neuroprotective Effects of HupA on Ab-associated Neurotoxicity"
"HupA may not only
ameliorate the cholinergic deficits, but also be capable of slowing down the progression
of disease by protecting the neurons from toxic insults. This would be beneficial to the
therapy of neurodegenerative diseases such as AD. In addition, understanding the
mechanisms of HupA actions may also provide valuable clues to aid the development of
new therapeutic agents for AD."
Acknowledgement This work was supported by grants from the Ministry of Science and Technology of
China (G199805110, G1998051115, 2004CB518907) and the National Natural Science Foundation of
China (39170860, 39770846, 3001161954, 30123005, 30271494 and 30572169).
References
Alvarez A, Alarcon R, Opazo C, Campos EO, Munoz FJ, Calderon FH, Dajas F, Gentry MK, Doctor,
BP, De Mello FG, Inestrosa NC (1998) Stable complexes involving acetylcholinesterase and
amyloid-beta peptide change the biochemical properties of the enzyme and increase the
neurotoxicity of Alzheimer’s fibrils. J Neurosci 18:3213–3223
Alvarez A, Opazo C, Alarcon R, Garrido J, Inestrosa NC (1997) Acetylcholinesterase promotes the
aggregation of amyloid-beta-peptide fragments by forming a complex with the growing fibrils. J Mol
Biol 272:348–361
Well here we are thanks to hedgehog.
LongeCity
