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Huperzine A improves cognitive deficits caused by chronic cerebral hypoperfusion in rats. Wang LM, Han YF, Tang XC. State Key Laboratory
of Drug Research, Shanghai Institute of Materia Medica, Chinese
Academy of Sciences, 200031, Shanghai, People's Republic of China. The effects of (-)-huperzine
A, a promising therapeutic agent for Alzheimer's disease, on
learning behavior and on alterations of the cholinergic system, the
oxygen free radicals and energy metabolites induced by permanent
bilateral ligation of the common carotid arteries were investigated
in rats. Daily oral administration of huperzine A produced a
significant improvement of the deficit in the learning of the water
maze task, beginning 28 days after ischemia, correlating to about
33-40% inhibition of acetylcholinesterase activity in cortex and
hippocampus. Huperzine A significantly restored the decrease in
choline acetyltransferase activity in hippocampus and significantly
reduced the increases in superoxide dismutase, lipid peroxide,
lactate and glucose to their normal levels. The present findings
demonstrate that the improvement by huperzine A of the cognitive
dysfunction in the late phase in chronically hypoperfused rats is
due to its effects, not only on the cholinergic system, but also on
the oxygen free radical system and energy metabolism. Our results
strongly suggest that huperzine A has therapeutic potential for the
treatment of dementia caused by cholinergic dysfunction and/or
decrease of cerebral blood flow.
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