Hock Christoph, Konietzko Uwe, Papassotiropoulos Andreas, Wollmer Axel, Streffer Johannes, von Rotz Ruth C, Davey Gabriela, Moritz Eva, Nitsch Roger M
Division of Psychiatry Research, University of Zurich, Zurich, Switzerland.
Nat Med. 2002 Nov;8(11):1270-5. doi: 10.1038/nm783. Epub 2002 Oct 15.
To characterize antibodies produced in humans in response to Abeta42 vaccination, we carried out immunohistochemical examinations of the brains of both transgenic mice and human patients with beta-amyloid pathology. We collected sera from patients with Alzheimer disease who received a primary injection of pre-aggregated Abeta42 followed by one booster injection in a placebo-controlled study. Antibodies in immune sera recognized beta-amyloid plaques, diffuse Abeta deposits and vascular beta-amyloid in brain blood vessels. The antibodies did not cross-react with native full-length beta-amyloid precursor protein or its physiological derivatives, including soluble Abeta42. These findings indicate that vaccination of AD patients with Abeta42 induces antibodies that have a high degree of selectivity for the pathogenic target structures. Whether vaccination to produce antibodies against beta-amyloid will halt the cognitive decline in AD will depend upon clinical assessments over time.
为了表征人类针对β淀粉样蛋白42（Aβ42）疫苗接种产生的抗体，我们对转基因小鼠和患有β淀粉样蛋白病变的人类患者的大脑进行了免疫组织化学检查。在一项安慰剂对照研究中，我们收集了接受初次注射预聚集Aβ42并随后进行一次加强注射的阿尔茨海默病患者的血清。免疫血清中的抗体识别大脑血管中的β淀粉样斑块、弥漫性Aβ沉积物和血管β淀粉样蛋白。这些抗体与天然全长β淀粉样前体蛋白或其生理衍生物（包括可溶性Aβ42）无交叉反应。这些发现表明，用Aβ42对阿尔茨海默病患者进行疫苗接种可诱导对致病靶结构具有高度选择性的抗体。通过接种疫苗产生针对β淀粉样蛋白的抗体是否会阻止阿尔茨海默病患者的认知衰退，将取决于长期的临床评估。
