Protective Effect And Pharmacological Significance Of Na～+-Ca～(2+) Exchanger In Heart/Brain Ischemia And β-amyloid Peptide Neurotoxicity

Cardiovascular and cerebral disease is the No.1 'killer' nowadays. Reperfusion during early stage of heart/brain ischemia can somewhat save the ischemic cells and decrease the area of infarction. However, reperfusion after that stage brings more serious injury, and may lead to arrhythmia, cellular stunning and necrosis.While Alzheimer's disease (AD) is a progressive neurodegenerative disease whose cause is still not clear and is characterized by learning and memory deficiency. Those brain regions related to advanced intelligence, especially the neocortex and hippocampus are highly susceptible during the whole pathological changes of AD. The accumulation of P-amyloid is widely accepted as its central etiological process. All known mutations that cause AD are followed by the significant production of P-amyloid. The essential part of P-amyloid is its residue of 25-35, namely Aβ_25-35, which can aggregate into fibril in vivo and in vitro. When Aβ_25-35 forms into β-sheet, it will be neurotoxic.The hypothesis of 'intracellular Ca²⁺ overload' concerning the injury caused by reperfusion and the Aβ_25-35 neurotoxicity has become the focus in recent years. And it has been determined that the Na⁺-Ca²⁺ exchanger in excitable cells plays a prominent role in regulation of intracellular Ca²⁺ homeostasis; the reverse mode of...