Hsieh Pei-Feng, Tsai Hsin-Hsi, Liu Chia-Ju, Lee Bo-Ching, Tsai Ya-Chin, Yen Ruoh-Fang, Jeng Jiann-Shing, Tsai Li-Kai
Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Department of Neurology, National Taiwan University Hospital Hsin-Chu Branch, Hsin-Chu, Taiwan.
Eur J Neurol. 2025 Feb;32(2):e70066. doi: 10.1111/ene.70066.
Blood-based biomarkers may offer a non-invasive approach to diagnose cerebral amyloid angiopathy (CAA), especially in early-stage. We evaluated the ability of plasma phosphorylated tau-217 (p-tau 217) to differentiate CAA from Alzheimer's disease (AD) and deep perforator arteriopathy (DPA).
Patients with AD (age 73.7 ± 8.1 years), probable CAA (74.8 ± 6.9 years), or DPA (66.1 ± 10.4 years) were enrolled from memory and stroke clinics at a medical center in Taiwan. All participants received amyloid and tau PET scans. Plasma biomarkers were measured via a SIMOA immunoassay platform. The diagnostic utility of p-tau 217 was assessed using ROC analyses and the Youden cutoff. Associations between plasma p-tau 217 and neuroimaging variables in CAA were explored.
Patients with CAA had lower plasma p-tau 217 (0.69 ± 0.76 vs. 1.28 ± 0.97 pg/mL, p < 0.001) and a lower p-tau 217/Aβ40 ratio (0.003 ± 0.002 vs. 0.006 ± 0.003, p < 0.001) than the AD group but higher levels than the DPA group (p-tau 217, 0.27 ± 0.13 pg/mL, p = 0.001; p-tau 217/Aβ40, 0.001 ± 0.0005, p < 0.001), although adjustment attenuated the difference in p-tau 217 between CAA and DPA. Plasma Aβ40, Aβ42, and Aβ40/Aβ42 were not significantly different between groups. Plasma p-tau 217 had moderate to good diagnostic utility to differentiate CAA vs. AD (sensitivity, 64.4%; specificity, 89.5%; AUC, 0.809) and CAA vs. DPA (sensitivity, 67.8%; specificity, 100%; AUC, 0.855). In CAA, p-tau 217 significantly correlated with the severity of CAA, amyloid PET signal intensity, and lobar microbleed count (p < 0.001).
Plasma p-tau 217 may represent a non-invasive biomarker for distinguishing cerebral amyloid angiopathy (CAA) from other conditions, including AD and DPA.
基于血液的生物标志物可能为诊断脑淀粉样血管病（CAA）提供一种非侵入性方法，尤其是在疾病早期。我们评估了血浆磷酸化tau-217（p-tau 217）区分CAA与阿尔茨海默病（AD）和深部穿支动脉病变（DPA）的能力。
从台湾某医疗中心的记忆和中风诊所招募了患有AD（年龄73.7±8.1岁）、可能的CAA（74.8±6.9岁）或DPA（66.1±10.4岁）的患者。所有参与者均接受了淀粉样蛋白和tau PET扫描。通过SIMOA免疫分析平台测量血浆生物标志物。使用ROC分析和尤登指数临界值评估p-tau 217的诊断效用。探讨了CAA患者血浆p-tau 217与神经影像学变量之间的关联。
与AD组相比，CAA患者的血浆p-tau 217水平较低（0.69±0.76 vs. 1.28±0.97 pg/mL，p<0.001），p-tau 217/Aβ40比值也较低（0.003±0.002 vs. 0.006±0.003，p<0.001），但高于DPA组（p-tau 217，0.27±0.13 pg/mL，p = 0.001；p-tau 217/Aβ40，0.001±0.0005，p<0.001），尽管调整后减弱了CAA与DPA之间p-tau 217的差异。各组之间血浆Aβ40、Aβ42和Aβ40/Aβ42无显著差异。血浆p-tau 217在区分CAA与AD（敏感性64.4%；特异性89.5%；AUC 0.809）以及CAA与DPA（敏感性67.8%；特异性100%；AUC 0.855）方面具有中度至良好的诊断效用。在CAA中，p-tau 217与CAA的严重程度、淀粉样蛋白PET信号强度和脑叶微出血计数显著相关（p<0.001）。
血浆p-tau 217可能是一种用于区分脑淀粉样血管病（CAA）与其他疾病（包括AD和DPA）的非侵入性生物标志物。
