{beta}-Amyloid-induced neurodegeneration and protection by structurally diverse microtubule-stabilizing agents

The Journal of Pharmacology and Experimental Therapeutics
Mary L MichaelisGunda Georg

Abstract

Deposition of beta-amyloid peptide (Abeta) and hyperphosphorylation of the tau protein are associated with neuronal dysfunction and cell death in Alzheimer's disease. Although the relationship between these two processes is not yet understood, studies have shown that both in vitro and in vivo exposure of neurons to Abeta leads to tau hyperphosphorylation and neuronal dystrophy. We previously reported that the microtubule-stabilizing drug paclitaxel (Taxol) protects primary neurons against toxicity induced by the Abeta(25-35) peptide. The studies in this report were undertaken to characterize the actions of paclitaxel more fully, to assess the effectiveness of structurally diverse microtubulestabilizing agents in protecting neurons, and to determine the time course of the protective effects of the drugs. Primary neurons were exposed to Abeta in the presence or absence of several agents shown to interact with microtubules, and neuronal survival was monitored. Paclitaxel protected neurons against Abeta(1-42) toxicity, and paclitaxel-treated cultures exposed to Abeta showed enhanced survival over Abeta-only cultures for several days. Neuronal apoptosis induced by Abeta was blocked by paclitaxel. Other taxanes and three structurally...Continue Reading

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