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阿尔茨海默氏病和多发性硬化症:通过病毒性脱髓化神经退行性触发物 (vDENT) 可能存在联系
Marina S Boukhvalova1, Lorne Kastrukoff2, Jorge C G Blanco1
1Sigmovir Biosystems, Inc., Rockville, MD, United States.
Frontiers in aging neuroscience
|July 3, 2023
概括
一个拟议的病毒触发模型表明,像HSV-1这样的早期病毒感染可能会导致脱髓化,导致多发性硬化症 (MS) 和后来的阿尔茨海默病.
科学领域:
- 神经科学和免疫学 神经科学和免疫学
- 传染病和神经退行性疾病
背景情况:
- 阿尔茨海默病 (AD) 和多发性硬化症 (MS) 是普遍存在的中枢神经系统疾病,缺乏治愈方法.
- 目前针对粉样蛋白或免疫路径的治疗方法取得了有限的成功,突显了了解疾病病因学的差距.
- 越来越多的证据表明,传染病原体,特别是病毒,可能在神经退行性和脱髓性疾病中发挥作用.
研究的目的:
- 提出一个统一的模型,病毒性DEmyelinating神经退行性触发器 (vDENT),通过共同的病毒病因和脱髓化,将MS和AD联系起来.
- 探索早期的病毒感染如何可以启动一连串导致晚年MS和AD.
主要方法:
- 概念模型开发 (vDENT) 基于病毒感染,脱髓化和神经退行现有证据.
- 在MS (脱,炎症) 和AD (粉样蛋白积累,神经退行) 中集成已知的病理机制.
- 假设从初始脱髓化进展到晚年AD痴呆症的进展.
主要成果:
- 根据vDENT模型,最初的脱髓化病毒感染 (例如HSV-1) 会引发早期的脱髓化.
- 随后的病毒再激活和炎症反应有助于复发性复发性多发性硬化症 (RRMS).
- 累积的损伤和病毒进展,结合与年龄相关的因素,促进粉样蛋白功能障碍和AD痴呆症.
结论:
- 病毒感染和随后的脱髓化可能是MS和AD病原体的共同途径.
- 针对生命早期病毒事件的干预措施可能会预防或延迟MS和AD的发病.
- 这种模型为开发对这些衰弱的中枢神经系统疾病的双效治疗策略提供了新的视角.
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