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Background The characteristic pathological changes of Alzheimer’s disease (AD) include extracellular deposits of b-amyloid protein (Ab) in brain, intracellular neurofibrillary tangles (NFTs), as well as a few neuronal loss. Several lines of evidence show that, neurotoxicity, such as Ab, glutamate, and oxidative stress, can lead to calcium influx, then induce the cleavage of P35 into P25. P25 is not readily degraded, and binding of p25 to Cyclin-dependent kinase 5 (Cdk5) constitutively activates Cdk5, changes its cellular location and alters its substrate specificity. The findings indicated that the p25/Cdk5 complex hyperphosphorylates tau which diminishes tau’s ability to associate with microtubules, disrupts the cytoskeleton and promotes the apoptosis of neurons. The level of P25 have been found to be elevated in brain of AD and overexpression of P25 in a transgenic mouse results in the formation of phosphorylated tau, neurofibrillary tangles and cognitive deficits. Thus, reducing intracellular calcium ion concentration, inhibiting the cleavage of P35 into P25 may be a new target for AD. Tanshinone IIA(Tan IIA) is one of ingredients of Tanshinone, appears to have neuroprotective effects. Our previous study indicated that Tan IIA can reduce intracellular calcium ion concentration, and has antioxidant effects. Yet, we presumed that Tan IIA may have effects on neurodegenerative diseases, such as AD and so on.

The protective effects of TanIIA on neurotoxicity induced by β-amyloid protein through the Cdk5/P35 pathway in cultured primary neurons