在多发性硬化症的认知障碍
1Cellular and Molecular Signaling, New York, NY 10022, USA.
Bioengineering (Basel, Switzerland)
|July 29, 2023
概括
多发性硬化症 (MS) 是一个不断增长的认知损失的原因. 需要针对炎症和细胞存活途径的新疗法来对抗MS相关的痴呆症和认知衰退.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 代谢途径 代谢途径
背景情况:
- 多发性硬化症 (MS) 影响全球近300万,其特点是神经系统脱髓化.
- 多发性硬化症的患病率上升,越来越多地被认为是认知损失和痴呆症的原因.
- 目前的疾病修饰疗法可以控制复发和大脑体积损失,但不能控制疾病的进展或认知障碍.
研究的目的:
- 探索治疗MS相关认知障碍的创新策略.
- 研究参与MS炎症,免疫细胞激活和细胞存活的新途径.
- 确定与MS相关的痴呆症和认知损失的潜在治疗点.
主要方法:
- 审查的途径,包括编程细胞死亡,哺乳动物叉转录因子 (FoxOs),机械标的拉巴素 (mTOR),AMP激活蛋白激酶 (AMPK),和无声交配类型信息规则2同类1 (SIRT1).
- 检查阿波利波蛋白E (APOE-ε4) 和SARS-CoV-2在MS病变发生中的作用.
- 分析这些途径与细胞代谢之间的相互作用,特别是尼古丁胺胺氨基二核酸 (NAD+).
主要成果:
- 确定了影响MS炎症,免疫反应和细胞存活的相互关联的途径.
- 突出了包括NAD+在内的代谢途径在MS相关的细胞过程中的关键作用.
- 在特定的分子通路 (FoxOs,mTOR,AMPK,SIRT1) 和MS相关的认知功能障碍之间建立了联系.
结论:
- 了解这些复杂的途径为MS提供了新的治疗途径.
- 针对炎症,免疫激活和细胞存活机制可以预防或逆转MS患者的认知衰退.
- 对这些途径的进一步研究可能会导致MS诱导的痴呆症的新治疗方法.
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