Mark R J, Blanc E M, Mattson M P
Sanders-Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA.
Mol Neurobiol. 1996 Jun;12(3):211-24. doi: 10.1007/BF02755589.
Alzheimer's disease is a progressive neurodegenerative disorder that affects primarily learning and memory functions. There is significant neuronal loss and impairment of metabolic functioning in the temporal lobe, an area believed to be crucial for learning and memory tasks. Aggregated deposits of amyloid beta-peptide may have a causative role in the development and progression of AD. We review the cellular actions of A beta and how they can contribute to the cytotoxicity observed in AD. A beta causes plasma membrane lipid peroxidation, impairment of ion-motive ATPases, glutamate uptake, uncoupling of a G-protein linked receptor, and generation of reactive oxygen species. These effects contribute to the loss of intracellular calcium homeostasis reported in cultured neurons. Many cell types other than neurons show alterations in the Alzheimer's brain. The effects of A beta on these cell types is also reviewed.
阿尔茨海默病是一种进行性神经退行性疾病，主要影响学习和记忆功能。颞叶存在显著的神经元丧失和代谢功能受损，该区域被认为对学习和记忆任务至关重要。β-淀粉样肽的聚集沉积物可能在阿尔茨海默病的发生和发展中起致病作用。我们综述了β-淀粉样蛋白（Aβ）的细胞作用以及它们如何导致在阿尔茨海默病中观察到的细胞毒性。Aβ会导致质膜脂质过氧化、离子驱动ATP酶功能受损、谷氨酸摄取、G蛋白偶联受体解偶联以及活性氧的产生。这些作用导致了培养神经元中细胞内钙稳态的丧失。除神经元外，许多其他细胞类型在阿尔茨海默病患者大脑中也会出现改变。本文还综述了Aβ对这些细胞类型的影响。
