Smith Mark A, Drew Kelly L, Nunomura Akihiko, Takeda Atsushi, Hirai Keisuke, Zhu Xiongwei, Atwood Craig S, Raina Arun K, Rottkamp Catherine A, Sayre Lawrence M, Friedland Robert P, Perry George
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA.
Neurochem Int. 2002 May;40(6):527-31. doi: 10.1016/s0197-0186(01)00123-1.
Alzheimer disease (AD) is defined pathologically and diagnostically defined by amyloid-beta senile plaques and neurofibrillary tangles (NFT) composed of tau. From the time of their original description nearly a century ago, a major focus has been to understand the role that these lesions play in the pathogenesis of the disease. The majority favors the notion that these lesions cause the disease and therefore attempts at therapeutic intervention are focused on preventing lesions formation. However, this rationale may be misguided since new evidence from our laboratories and others suggest that the lesions not only occur as a by-product of the fundamental disease process but also that they may be protective.
阿尔茨海默病（AD）在病理上由β-淀粉样老年斑和由tau组成的神经原纤维缠结（NFT）定义，在诊断上也以此为依据。自近一个世纪前首次描述它们以来，一个主要关注点一直是了解这些病变在该疾病发病机制中所起的作用。大多数人倾向于认为这些病变会引发疾病，因此治疗干预的尝试集中在预防病变形成上。然而，这一基本原理可能是错误的，因为我们实验室和其他机构的新证据表明，这些病变不仅是基本疾病过程的副产品，而且它们可能具有保护作用。
