Alzheimer's disease:: Aβ, tau and synaptic dysfunction
Alzheimer's disease:: Aβ, tau and synaptic dysfunction
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DOI：
10.1016/j.molmed.2005.02.009
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发表时间：
2005-04-01
影响因子：
13.6
通讯作者：
Oddo, S
中科院分区：
文献类型：
--
作者：
LaFerla, FM;Oddo, S
阿尔茨海默病是一种进行性神经退行性疾病，其特征是两个标志性病变：细胞外淀粉样蛋白斑和神经原纤维缠结。事实证明，这些病变在 AD 发病机制中所起的作用很难阐明，部分原因是在转基因小鼠中复制这两种病理标志面临着意想不到的挑战。最近在重现转基因小鼠大脑中的斑块和缠结方面取得的进展，使人们对它们在退化过程中的作用，包括它们对突触活动和可塑性的影响有了新的认识。具有两种神经病理学病变的转基因小鼠也有助于阐明这些蛋白质聚集体彼此之间的关系，并为开发和评估疗法提供重要的体内系统。
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.