针对痴呆症的纤维素向免疫疗法
A B Kantor1, K Akassoglou, J B Stavenhagen
1Jeffrey Stavenhagen, PhD, Therini Bio, Inc, Sacramento, CA, USA,
The journal of prevention of Alzheimer's disease
|October 24, 2023
概括
血脑屏障的破坏允许纤维素素进入大脑,引发炎症和神经退行. 用THN391等抗体向纤维素P2表位,对治疗阿尔茨海默病和其他神经系统疾病有很大的前景.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 血脑屏障 (BBB) 的破坏是阿尔茨海默病发病的早期事件.
- 泄漏的纤维素素转化为纤维素,暴露P2表位,激活先天免疫细胞并引起神经炎症.
- 这种纤维素介导的炎症对神经元有毒,并与神经退行性疾病有关.
研究的目的:
- 调查纤维素P2表位在神经炎症和神经退行症中的作用.
- 评估用单克隆抗体向纤维素P2表位的治疗潜力.
主要方法:
- 使用小鼠单克隆抗体5B8,向纤维素P2表位.
- 评估了5B8在动物模型中减少神经退行和神经炎症的疗效.
- 开发了THN391,一种人性化的抗体,对纤维素P2有增强的亲和力.
主要成果:
- 抗体5B8在阿尔茨海默氏症和多发性硬化症模型中显示减少神经退行和神经炎症.
- THN391对纤维素P2的亲和力高出100倍,并且对5B8.8的性能有所改善.
- 目前,THN391正在进行1期临床试验.
结论:
- 向纤维素P2表位是神经退行性疾病的可行的治疗策略.
- 像THN391这样的单克隆抗体为治疗与BBB干扰和神经炎症相关的疾病提供了有希望的方法.
- 需要对THN391进行进一步的临床研究.
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