Lan Guoyu, Zhang Laihong, Li Anqi, Ran Wenqing, Lv Jieqin, Gonzalez-Ortiz Fernando, Cai Yue, Sun Pan, Liu Lin, Yang Jie, He Zhengbo, Fang Lili, Zhou Xin, Zhu Yalin, Liu Zhen, Chen Xuhui, Fan Xiang, Shi Dai, Ye Chenghui, Xu Linsen, Wang Qingyong, Blennow Kaj, Cheng Guanxun, Ran Pengcheng, Wang Lu, Guo Tengfei
Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
School of Biology and Biological Engineering, South China University of Technology, Guangzhou, China.
Alzheimers Dement. 2025 Mar;21(3):e14550. doi: 10.1002/alz.14550. Epub 2025 Jan 17.
Novel fluid biomarkers for tracking neurodegeneration specific to Alzheimer's disease (AD) are greatly needed.
Using two independent well-characterized cohorts (n = 881 in total), we investigated the group differences in plasma N-terminal tau (NT1-tau) fragments across different AD stages and their association with cross-sectional and longitudinal amyloid beta (Aβ) plaques, tau tangles, brain atrophy, and cognitive decline.
Plasma NT1-tau significantly increased in symptomatic AD and displayed positive associations with Aβ PET (positron emission tomography) and tau PET. Higher baseline NT1-tau levels predicted greater tau PET, with 2- to 10-year intervals and faster longitudinal Aβ PET increases, AD-typical neurodegeneration, and cognitive decline. Plasma NT1-tau showed negative correlations with baseline regional brain volume and thickness, superior to plasma brain-derived tau (BD-tau) and neurofilament light (NfL) in Aβ-positive participants.
This study suggests that plasma NT1-tau is an Aβ-dependent biomarker and outperforms BD-tau and NfL in detecting cross-sectional neurodegeneration in the AD continuum.
Plasma N-terminal tau (NT1-tau) was specifically increased in the A+/T+ stage. Plasma NT1-tau was positively associated with greater amyloid beta (Aβ) and tau PET (positron emission tomography) accumulations. Higher plasma NT1-tau predicted greater tau burden and faster Aβ increases. Plasma NT1-tau was more related to neurodegeneration than plasma brain-derived tau (BD-tau) and neurofilament light (NfL).
非常需要用于追踪阿尔茨海默病（AD）特有的神经退行性变的新型流体生物标志物。
我们使用两个独立且特征明确的队列（总共n = 881），研究了不同AD阶段血浆N端tau（NT1-tau）片段的组间差异及其与横断面和纵向淀粉样β（Aβ）斑块、tau缠结、脑萎缩和认知衰退的关联。
有症状的AD患者血浆NT1-tau显著升高，并与Aβ正电子发射断层扫描（PET）和tau PET呈正相关。较高的基线NT1-tau水平预示着tau PET更高，间隔2至10年且纵向Aβ PET增加更快，出现AD典型的神经退行性变和认知衰退。在Aβ阳性参与者中，血浆NT1-tau与基线区域脑体积和厚度呈负相关，优于血浆脑源性tau（BD-tau）和神经丝轻链（NfL）。
本研究表明血浆NT1-tau是一种Aβ依赖性生物标志物，在检测AD连续体中的横断面神经退行性变方面优于BD-tau和NfL。
血浆N端tau（NT1-tau）在A+/T+阶段特异性升高。血浆NT1-tau与更大的淀粉样β（Aβ）和tau正电子发射断层扫描（PET）积累呈正相关。较高的血浆NT1-tau预示着更大的tau负担和更快的Aβ增加。与血浆脑源性tau（BD-tau）和神经丝轻链（NfL）相比，血浆NT1-tau与神经退行性变的关系更大。
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