Rogers J, Cooper N R, Webster S, Schultz J, McGeer P L, Styren S D, Civin W H, Brachova L, Bradt B, Ward P
L. J. Roberts Center, Sun Health Research Institute, Sun City, AZ 85351.
Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10016-20. doi: 10.1073/pnas.89.21.10016.
Alzheimer disease (AD) is characterized by excessive deposition of the beta-amyloid peptide (beta-AP) in the central nervous system. Although several lines of evidence suggest that beta-AP is neurotoxic, a mechanism for beta-AP toxicity in AD brain remains unclear. In this paper we provide both direct in vitro evidence that beta-AP can bind and activate the classical complement cytolytic pathway in the absence of antibody and indirect in situ evidence that such actions occur in the AD brain in association with areas of AD pathology.
阿尔茨海默病（AD）的特征是β-淀粉样肽（β-AP）在中枢神经系统中过度沉积。尽管有几条证据表明β-AP具有神经毒性，但AD脑中β-AP毒性的机制仍不清楚。在本文中，我们既提供了直接的体外证据，表明β-AP在没有抗体的情况下可以结合并激活经典补体溶细胞途径，也提供了间接的原位证据，表明这种作用在AD脑中与AD病理区域相关联时发生。
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