β-Amyloid Protein Damaged The Neural Cells And Protector Inhibited This Damaging And The Signal Transduction In This Process

With the development of the society, people get longevity and the incidence of Alzheimer's disease (AD) increased. AD can cause great trouble for the whole society, the families and the individuals. So, investigation of AD became the research focus all over the world. Although we had some knowledge of the etiology, gene location, diagnosis and therapy of AD, there are still a lot of unknown field about AD need to be done. The major component of the neuritic plaques (it was called as senile plaques in the past) and the amyloid angiopathy is P-amyloid protein, which is degraded from amyloid protein precusor(APP). P-amyloid protein consists of 39-42 amino acids and the active section is in the 25^th-35^th amino acid residues (GSNKGAIIGLM)^[1].Because there is no appropriate animal model for AD investigation, so we often use SH-SY5Y cell as the investigation object. In this article, we observed that after the stimulation of the Aβ25-35,the biochemical change and the change of a certain enzyme, caspase-3, which is an important enzyme in the signal transduction; we also observed that vitmine E—an antioxidant and nimodipine—calcium channel blocker, could counteract the damage caused by Aβ25-35,so vitmine E and nimodipine could protect the SH-SY5Y cells.In the first part of this article, we detected apoptosis by fluorescence...