Alzheimer's disease:: Aβ, tau and synaptic dysfunction

被引:366
作者
LaFerla, FM [1 ]
Oddo, S [1 ]
机构
[1] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA
关键词
D O I
10.1016/j.molmed.2005.02.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alzheimer's disease is a progressive neurodegenerative disorder that is characterized by two hallmark lesions: extracellular amyloid plaques and neurofibrillary tangles. The role that these lesions have in the pathogenesis of AD has proven difficult to unravel, in part because of unanticipated challenges of reproducing both pathologic hallmarks in transgenic mice. Recent advances in recapitulating both plaques and tangles in the brains of transgenic mice are leading to novel insights into their role in the degenerative process, including their impact on synaptic activity and plasticity. Transgenic mice that harbor both neuropathological lesions are also facilitating the elucidation of the relationship of these proteinaceous aggregates to one another and providing a crucial in vivo system for developing and evaluating therapies.
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收藏
页码:170 / 176
页数:7
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