Butterfield D Allan
Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506-0055, USA.
Curr Med Chem. 2003 Dec;10(24):2651-9. doi: 10.2174/0929867033456422.
In addition to synapse loss, neurofibrillary tangles, and neurodegeneration, oxidative stress and amyloid beta-peptide [Abeta] deposition are hallmarks of Alzheimer's disease [AD] brain. Our laboratory coupled these two characteristics of AD into a comprehensive model to account for the synapse loss and neurodegeneration in AD brain. This model combines much of the extant studies on AD and is based on oxidative stress associated with amyloid beta-peptide. This review presents evidence in support of this model and provides insight into the molecular basis of this devastating dementing disorder.
除了突触丧失、神经原纤维缠结和神经退行性变外，氧化应激和β-淀粉样肽（Aβ）沉积是阿尔茨海默病（AD）脑的特征。我们实验室将AD的这两个特征整合到一个综合模型中，以解释AD脑中的突触丧失和神经退行性变。该模型结合了许多关于AD的现有研究，并基于与β-淀粉样肽相关的氧化应激。这篇综述提供了支持该模型的证据，并深入探讨了这种毁灭性痴呆症的分子基础。
