Longitudinal plasma p-tau217 is increased in early stages of Alzheimer's disease.
Longitudinal plasma p-tau217 is increased in early stages of Alzheimer's disease.
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DOI：
10.1093/brain/awaa286
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发表时间：
2020-12-05
期刊：
影响因子：
--
通讯作者：
Hansson O
中科院分区：
文献类型：
--
作者：
Mattsson-Carlgren N;Janelidze S;Palmqvist S;Cullen N;Svenningsson AL;Strandberg O;Mengel D;Walsh DM;Stomrud E;Dage JL;Hansson O
参见Teunissen et al.（doi：）关于这篇文章的科学评论。血浆磷酸化tau蛋白（p-tau 217）是阿尔茨海默病的一个有前途的新生物标志物，但尚未进行纵向研究。Mattsson-Carlgren等人表明，在临床前和前驱阿尔茨海默病中，水平随着时间的推移而增加，这表明适合作为跟踪疾病发展的微创工具。在苏氨酸-217（p-tau 217）处磷酸化的tau的血浆水平是监测阿尔茨海默病的候选工具。我们研究了瑞典BioFINDER研究中的150名认知未受损参与者和100名轻度认知障碍患者。重复测量P-tau 217长达6年（平均每人三个样本，从第一个到最后一个样本的平均时间为4.3年）。临床前（淀粉样蛋白-β阳性认知未受损，n = 62）和前驱症状（淀粉样蛋白-β阳性轻度认知障碍，n = 49）与淀粉样蛋白-β阴性认知未受损相比，阿尔茨海默病加速了p-tau 217（β = 0.56，P < 0.001，采用线性混合效应模型）和淀粉样蛋白阴性轻度认知功能障碍患者（β = 0.67，P < 0.001）。与其他轻度认知障碍患者相比，后来转化为阿尔茨海默病痴呆的轻度认知障碍患者（n = 40）具有加速的p-tau 217（β = 0.79，P < 0.001）。P-tau 217在淀粉样蛋白-β阴性参与者中没有变化，或者在没有转化为阿尔茨海默病痴呆的轻度认知障碍患者中没有变化。对于80%的把握度，每组需要109名参与者观察淀粉样蛋白-β阳性认知未受损的斜率降低（每组71名参与者为淀粉样蛋白-β阳性轻度认知障碍）。p-tau 217的纵向增加与认知和脑萎缩的纵向恶化相关。总之，血浆p-tau 217在早期阿尔茨海默病期间增加，可用于监测疾病进展。
See Teunissen et al. (doi:) for a scientific commentary on this article. Plasma phosphorylated tau (p-tau217) is a promising new biomarker for Alzheimer’s disease, but has yet to be studied longitudinally. Mattsson-Carlgren et al. show that levels increase over time in preclinical and prodromal Alzheimer’s disease, suggesting suitability as a minimally invasive tool to track disease development. Plasma levels of tau phosphorylated at threonine-217 (p-tau217) is a candidate tool to monitor Alzheimer’s disease. We studied 150 cognitively unimpaired participants and 100 patients with mild cognitive impairment in the Swedish BioFINDER study. P-tau217 was measured repeatedly for up to 6 years (median three samples per person, median time from first to last sample, 4.3 years). Preclinical (amyloid-β-positive cognitively unimpaired, n = 62) and prodromal (amyloid-β-positive mild cognitive impairment, n = 49) Alzheimer’s disease had accelerated p-tau217 compared to amyloid-β-negative cognitively unimpaired (β = 0.56, P < 0.001, using linear mixed effects models) and amyloid-β-negative mild cognitive impairment patients (β = 0.67, P < 0.001), respectively. Mild cognitive impairment patients who later converted to Alzheimer’s disease dementia (n = 40) had accelerated p-tau217 compared to other mild cognitive impairment patients (β = 0.79, P < 0.001). P-tau217 did not change in amyloid-β-negative participants, or in patients with mild cognitive impairment who did not convert to Alzheimer’s disease dementia. For 80% power, 109 participants per arm were required to observe a slope reduction in amyloid-β-positive cognitively unimpaired (71 participants per arm in amyloid-β-positive mild cognitive impairment). Longitudinal increases in p-tau217 correlated with longitudinal worsening of cognition and brain atrophy. In summary, plasma p-tau217 increases during early Alzheimer’s disease and can be used to monitor disease progression.
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影响因子：
29
作者：
Donohue, Michael C.;Sperling, Reisa A.;Salmon, David P.;Rentz, Dorene M.;Raman, Rema;Thomas, Ronald G.;Weiner, Michael;Aisen, Paul S.
通讯作者：
Aisen, Paul S.
影响因子：
5.3
作者：
Janelidze S;Zetterberg H;Mattsson N;Palmqvist S;Vanderstichele H;Lindberg O;van Westen D;Stomrud E;Minthon L;Blennow K;Swedish BioFINDER study group;Hansson O
通讯作者：
Hansson O
影响因子：
5.7
作者：
Reuter, Martin;Schmansky, Nicholas J.;Rosas, H. Diana;Fischl, Bruce
通讯作者：
Fischl, Bruce
影响因子：
82.9
作者：
Thijssen, Elisabeth H.;La Joie, Renaud;Boxer, Adam L.
通讯作者：
Boxer, Adam L.
影响因子：
29
作者：
Mattsson N;Andreasson U;Zetterberg H;Blennow K;Alzheimer’s Disease Neuroimaging Initiative
通讯作者：
Alzheimer’s Disease Neuroimaging Initiative