Linking Abeta and tau in late-onset Alzheimer's disease: a dual pathway hypothesis.
摘要：
Alzheimer's disease is characterized by abnormal elevation of Aβ peptide and abnormal hyperphosphorylation of the tau protein. The "amyloid hypothesis," which is based on molecular defects observed in autosomal-dominant early-onset Alzheimer's disease (EOAD), suggests a serial model of causality, whereby elevation of Aβ drives other disease features including tau hyperphosphorylation. Here, we review recent evidence from drug trials, genetic studies, and experimental work in animal models that suggests that an alternative model might exist in late-onset AD (LOAD), the complex and more common form of the disease. Specifically, we hypothesize a "dual pathway" model of causality, whereby Aβ and tau can be linked by separate mechanisms driven by a common upstream driver. This model may account for the results of recent drug trials and, if confirmed, may guide future drug development.
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关键词：
Alzheimer Disease Amyloid beta-Protein Animals Apolipoprotein E4 Brain 淀粉样β蛋白 动物 脑 疾病遗传易感性 模型, 神经学
DOI：
10.1016/j.neuron.2008.11.007
被引量：
年份：
2008
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