生物标志物 生物标志物
Nicole S McKay1, Stephanie Doering2, David A Hoagey2
1Washington University in St. Louis, School of Medicine, St. Louis, MO, USA.
Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 26, 2025
概括
自体主导性阿尔茨海默病 (ADAD) 中的白质损伤在症状出现前几年就开始,特别是在与病理相关的特定脑道中. 这种早期的衰退凸显了陶氏在推动ADAD进展和认知衰退中的作用.
科学领域:
- 神经科学是一个神经科学.
- 神经病理学神经病理学
- 遗传学 遗传学 是一个
背景情况:
- 粉样和病态是阿尔茨海默病 (AD) 的关键,独特地通过子样传播驱动白质 (WM) 微结构损伤.
- 积和WM下降在临床症状之前,强调它们在AD表现中的关键作用.
- 自体主导AD (ADAD) 为研究临床前AD提供了一个模型,因为它具有统一的表型,早期病理学和精确的疾病分期.
研究的目的:
- 调查ADAD中积和白质微观结构完整性之间的临床前关系.
- 使用先进的神经成像技术,对ADAD突变载体和非载体的白质完整性进行表征.
- 为了确定白质异常相对于ADAD疾病发病的时间.
主要方法:
- 利用来自主导性遗传阿尔茨海默症网络 (DIAN) 的数据.
- 评估白质完整性使用分数异构,平均扩散率,轴向扩散率和辐射扩散率通过基于通道的空间统计.
- 进行了概率曲谱,从带束和无带束中提取白质指数,这些区域与积枢纽相关.
主要成果:
- 与无症状携带者和非携带者相比,具有ADAD突变携带者的全脑白质微观结构显著改变.
- 突变载体中的白质异常与症状进展同时出现.
- 管道特异性分析显示,与非携带者相比,所有突变载体的白质微观结构差异相比,在带膜束和未结合囊中,在预期的症状发作前五年出现.
结论:
- 在ADAD中,全球白质差异在症状开始时明显,但在积点附近的区域表现出更早的微观结构异常.
- 这表明ADAD白质量下降不均,并且与tau积累空间相关,损害发生在tau传播的下游.
- 描述和白质进展对于理解如何驱动ADAD的认知症状发作至关重要.
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