Horikoshi Yuko, Mori Takashi, Maeda Masahiro, Kinoshita Noriaki, Sato Kumiko, Yamaguchi Haruyasu
Gunma University School of Health Sciences, Maebashi, Gunma 371-8514, Japan.
Biochem Biophys Res Commun. 2004 Dec 10;325(2):384-7. doi: 10.1016/j.bbrc.2004.10.039.
Alzheimer's disease (AD) is a neurodegenerative disease with memory dysfunction that is causing serious medical problems in modern society. For the fundamental treatment of AD, an amyloid beta protein (Abeta) vaccine is considered to be the most potent candidate. To cure AD, we developed Abeta N-terminal-end specific monoclonal antibody named 82E1, which does not cross-react with full-length Abeta precursor. Passive intraperitoneal administration of 82E1 markedly reduced total plaque area (Abeta burden) in the Tg2576 mouse brains. This was confirmed by the ELISA measurement of insoluble Abeta in the brain homogenates. The density of diffuse plaques, which increases in the late stage, was markedly reduced by the administration of 82E1, suggesting that the reduction of the Abeta burden was due to the prevention of newly developed diffuse plaques. Above results provide an insight into the further therapeutic intervention in AD with few adverse effects.
阿尔茨海默病（AD）是一种伴有记忆功能障碍的神经退行性疾病，在现代社会中引发了严重的医学问题。对于AD的根本性治疗，β淀粉样蛋白（Aβ）疫苗被认为是最有潜力的候选方案。为了治愈AD，我们研发了一种名为82E1的Aβ N末端特异性单克隆抗体，它不会与全长Aβ前体发生交叉反应。向Tg2576小鼠脑内被动腹腔注射82E1可显著减少总斑块面积（Aβ负荷）。这通过对脑匀浆中不溶性Aβ进行ELISA检测得以证实。82E1给药后，晚期增加的弥漫性斑块密度显著降低，这表明Aβ负荷的降低是由于预防了新形成的弥漫性斑块。上述结果为进一步对AD进行几乎无不良反应的治疗干预提供了思路。
