@article {Sartoe860作者={乔迪Sarto和拉奎尔Ruiz-Garc{\ \我}和N {\ ' u} ria Guill {\ ' N e}和{\ ' O}疤痕Ramos-Campoy和该处赛场{\ '}s和戴安娜Esteller乔斯{\ ' e}康塔和瓜达卢佩蕨{\ '}ndez,尤兰达Gonz {\ '} lez Adri {\ '} Tort-Merino和乔迪接合{\ '}-Parella和Bea博世以及塞尔吉博雷戈,{\ ' e}比赛和劳拉Molina-Porcel和玛格达Castellv{\ \我}和米格尔·安娜Antonell约瑟Mar{8月\ \我}{}\ ' e和劳拉Naranjo和拉奎尔Sanchez-Valle和艾伯特Llad {\ ' O}和米尔卡Balasa}, title = {Blood-Based生物标志物的诊断性能和临床适用性前瞻记忆诊所队列},体积={100}={8},页面= {e860——e873} = {2023}, doi = {10.1212 / WNL。出版商0000000000201597}= {Wolters Kluwer健康,公司代表美国神经病学学会},文摘={背景和目标Blood-based生物标志物已成为微创的选择评估认知障碍。首页迄今为止,大多数研究评估他们在研究人群,限制日常临床实践的概括。我们评价他们的诊断性能和临床适用性。她们在一次前瞻性现实、记忆诊所队列。方法对所有的病人被怀疑是认知障碍2019年7月至2021年6月前瞻性邀请参加。五等离子体生物标志物(τ在苏氨酸磷酸化181 [p-tau181],胶质原纤维酸性蛋白(GFAP),神经丝轻链(NfL),总τ(t-tau)和泛素c端水解酶L1 [UCH-L1])测定与单分子阵列。性能评估相比,临床诊断(瞎了等离子体的结果)和淀粉样状态(CSF / PET)。一群没有认知能力受损(铜)控制也包括在内。结果三百四十九名参与者(平均年龄68,SD 8.3年)和36铜控制(平均年龄61.7岁,标准差8.2岁)被包括在内。在subcohort可用阿尔茨海默病(AD)生物标志物(n = 268),等离子体p-tau181和GFAP诊断精度高区分广告non-neurodegenerative原因(接受者操作特征曲线下面积0.94和0.92,分别),与p-tau181 GFAP表现系统。血浆p-tau181水平预测淀粉样状态(85 \ %敏感性和特异性)与准确的个人预测在大约60 \ %的患者。 Plasma NfL differentiated frontotemporal dementia (FTD) syndromes from CU (0.90) and non-neurodegenerative causes (0.93), whereas the discriminative capacity with AD and between all neurodegenerative and non-neurodegenerative causes was less accurate. A combination of p-tau181 and NfL identified FTD with 82\% sensitivity and 85\% specificity and had a negative predictive value for neurodegenerative diagnosis of 86\%, ruling out half of the non-neurodegenerative diagnoses. In the subcohort without AD biomarkers, similar results were obtained. T-tau and UCH-L1 did not offer added diagnostic value.Discussion Plasma p-tau181 predicted amyloid status with high accuracy and could have potentially avoided CSF/amyloid PET testing in approximately 60\% of subjects in a memory clinic setting. NfL was useful for identifying FTD from non-neurodegenerative causes but behaved worse than p-tau181 in all other comparisons. Combining p-tau181 and NfL improved diagnostic performance for FTD and non-neurodegenerative diagnoses. However, the 14\% false-negative results suggest that further improvement is needed before implementation outside memory clinics.Classification of Evidence This study provides Class I evidence that plasma p-tau181 correlates with the presence or absence of AD and a combination of plasma p-tau181 and NfL correlates moderately well with a diagnosis of FTD.Aβ=β-amyloid; AD=Alzheimer disease; AUC=area under the ROC curve; bvFTD=behavioral variant FTD; CBS=corticobasal syndrome; CJD=Creutzfeldt-Jakob disease; CU=cognitively unimpaired; FTD=frontotemporal dementia; GFAP=glial fibrillary acidic protein; LBD=Lewy body dementia; MCI=mild cognitive impairment; MMSE=Mini-Mental State Examination; NfL=neurofilament light chain; nfPPA=nonfluent variant PPA; NPV=negative predictive value; PM=parsimonious model; PPA=primary progressive aphasia; PPV=positive predictive value; PSP=progressive supranuclear palsy; p-tau181=tau phosphorylated at threonine 181; ROC=receiver operating characteristic; SCD=subjective cognitive decline; SiMoA=single-molecule array; SND=suspected nondegenerative cognitive impairment; svPPA=semantic variant PPA; t-tau=total tau; UCH-L1=ubiquitin C-terminal hydrolase L1}, issn = {0028-3878}, URL = {//www.ez-admanager.com/content/100/8/e860}, eprint = {//www.ez-admanager.com/content/100/8/e860.full.pdf}, journal = {Neurology} }