Division of Geriatric Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104, USA.
Curr Pharm Des. 2012;18(8):1123-30. doi: 10.2174/138161212799315795.
The senescence accelerate mouse P8 (SAMP8) is an excellent model of early learning and memory problems. A number of studies have shown that it has cholinergic deficits, oxidative damage, alterations in membrane lipids and circadian rhythm disturbances. The brains of the SAMP8 overproduce amyloid precursor protein (APP), amyloid-beta protein and have an increased physphorylation of tau. An antisense to APP has been developed that reverses the cognitive deficits and oxidative damage. This antisense represents a potential treatment for Alzheimer's disease.
衰老加速鼠 P8（SAMP8）是学习和记忆早期问题的优秀模型。许多研究表明，它存在胆碱能缺陷、氧化损伤、膜脂改变和昼夜节律紊乱。SAMP8 脑中过度产生淀粉样前体蛋白（APP）、β-淀粉样蛋白，并且 tau 发生过度磷酸化。已经开发出 APP 的反义寡核苷酸，可逆转认知缺陷和氧化损伤。这种反义寡核苷酸可能是阿尔茨海默病的一种治疗方法。
