中央自主网络功能障碍和老年人的血阿尔茨海默病生物标志物
Trevor Lohman1, Arunima Kapoor2, Allison C Engstrom2
1University of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA.
Alzheimer's research & therapy
|June 8, 2024
概括
这项研究发现,中央自主网络 (CAN) 功能连接与老年人阿尔茨海默病 (AD) 生物标志物有关. 较低的连接性与APOE4载体的粉样蛋白减少和GFAP增加相关,这表明AD风险的早期自主功能障碍.
科学领域:
- 神经科学是一个神经科学.
- 自主神经系统研究 自主神经系统研究
- 阿尔茨海默病生物标志物 阿尔茨海默病生物标志物
背景情况:
- 中央自主网络 (CAN) 通过协调的大脑区域来调节自主功能.
- 自主功能障碍在阿尔茨海默氏症 (AD) 和痴呆症中很常见.
- 没有先前的研究将血AD生物标志物与高危老年人中的CAN功能连接性联系起来.
研究的目的:
- 调查血AD生物标志物与高危老年人CAN功能连接之间的关联.
- 探索特定的AD生物标志物 (粉样蛋白,NfL,GFAP) 与自主网络连接之间的关系.
- 检查APOE4载体身份在这些协会中的调节作用.
主要方法:
- 招募了122名独立生活的老年人,没有主要的神经/精神疾病.
- 使用静止状态fMRI来评估CAN和传感器运动网络连接.
- 测量了Aβ42,Aβ40,NfL和GFAP的血水平;使用多重线性回归分析了相关性.
主要成果:
- 所有自主网络与Aβ42/40比率正相关.
- 总体和副交感CAN网络显示了与GFAP的负面关联.
- 具有低副交感CAN连接性的APOE4载体具有最高GFAP水平.
结论:
- CAN功能连接与血AD生物标志物水平有关.
- 较低的CAN连接与AD风险的APOE4载体的Aβ42/40降低和GFAP增加有关.
- 研究结果表明,在阿尔茨海默病早期阶段,可能存在更高阶级的自主功能障碍.
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