(-)Clausenamide Improves Learing And Memory Deficits Induced By β-amyloid Peptide Infusion And In Aged Rats And Its Inhibitory Action On Tau Protein Hyperphosphorylation In STZ Induced Diabetic Mice

Alzheimer's disease, a neuro-degeneration disease, is the most common disease occurred in aged people. The main clinical symptoms of AD are progressive cognitive decline and mental deterioration. AD is neuropathologyically characterized by senile plaque composed by amyloid protein depositions, neurofibrillary tangle and neuron loss in nervous system.Clausenamide is a new compound isolated from Clausena Lansium Lour Skells, and its natural structure is similar to piracetam and now is synthesized and can be resoluted into (-) and (+) clausenamide. In previous pharmacological studies indicated that (-) clausenamide had neuroprotective effects in central nervous system, but (+)clausenamide has no pharmacological effects.In this study, we observed the (-) clausenamide's pharmacological effects in various AD's pathological models in vitro and in vivo, such as β -amyloid protein (A β ) toxicity in PC12 cells, continuous intracerebroventricular infusion of β -amyloid (1-40) in rats, aged rat, tau protein hyperphosphorylation in diabetes mice.