Opening of the Mitochondrial Permeability Transition Pore by Reactive Oxygen Species is a Basic Event in Neurodegeneration

摘要

This addendum concludes the work on the neurotoxicity induced by A% beta which was an extension of our original work involving the administration of aluminum maltolate into rabbit brain. The intracisternal injection of A beta(1- 42) induces apoptosis and phosphorylation of tau in the hippocampus of New Zealand white rabbits. These A beta effects correlate with the activation of JNK, ERK, c-jun and c-fos, but not of p38. Treatment with 7 mM lithium inhibits apoptosis, prevents the activation of JNK and c-jun, increases the activation of ERK and c-fos, and does not affect tau.