Neuropathology and treatment of Alzheimer disease: did we lose the forest for the trees?
Neuropathology and treatment of Alzheimer disease: did we lose the forest for the trees?
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DOI：
10.1586/14737175.7.5.473
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发表时间：
2007-05-01
影响因子：
4.3
通讯作者：
Smith, Mark A
中科院分区：
文献类型：
--
作者：
Castellani, Rudy J;Zhu, Xiongwei;Smith, Mark A
尽管含有β-淀粉样蛋白的老年斑和含有磷酸tau蛋白的神经原纤维缠结是阿尔茨海默病(AD)的标志性病变，但这两者都不是AD特有的，甚至也不是AD的标志物。相反，它们是经验性病变，需要与年龄和临床体征密切相关才能获得最佳解释。从本质上讲，这些病变代表了疾病的结果而不是原因。在这篇综述中，我们讨论了 AD 的诊断标准、病理学、发病机制和迄今为止令人失望的多种治疗方法之间的关系，包括那些假定解决病理病变的方法。接受基于病变的治疗不能解决病因或限速致病因素的观点可能是取得迄今为止难以实现的重大进展的最佳机会所必需的。
Although amyloid-beta-containing senile plaques and phospho-tau containing neurofibrillary tangles are hallmark lesions of Alzheimer disease (AD), neither is specific for AD, nor even a marker of AD. Rather, they are empirical lesions that require close correlation with age and clinical signs for optimal interpretation. In essence, these lesions represent the effect rather than the cause of disease. In this review, we discuss diagnostic criteria for AD, the relationship between pathology, pathogenesis and multiple treatment approaches that have so far been disappointing, including those that presume to address pathological lesions. An acceptance that lesion-based therapies do not address etiology or rate-limiting pathogenic factors is probably necessary for the best chance of significant advances that have thus far been elusive.