Plasma neurofilament light, glial fibrillary acid protein, and phosphorylated tau 181 as biomarkers for neuropsychiatric symptoms and related clinical disease progression.

IF 7.9 1区 医学 Q1 CLINICAL NEUROLOGY Alzheimer's Research & Therapy Pub Date : 2024-07-25 DOI:10.1186/s13195-024-01526-4
Miriam Rabl, Leonardo Zullo, Piotr Lewczuk, Johannes Kornhuber, Thomas K Karikari, Kaj Blennow, Henrik Zetterberg, Francesco Bavato, Boris B Quednow, Erich Seifritz, Armin von Gunten, Christopher Clark, Julius Popp
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Abstract

Background: Neuropsychiatric symptoms (NPS) are common in older people, may occur early in the development of dementia disorders, and have been associated with faster cognitive decline. Here, our objectives were to investigate whether plasma levels of neurofilament light chain (NfL), glial fibrillary acid protein (GFAP), and tau phosphorylated at threonine 181 (pTau181) are associated with current NPS and predict future NPS in non-demented older people. Furthermore, we tested whether the presence of NPS combined with plasma biomarkers are useful to predict Alzheimer's disease (AD) pathology and cognitive decline.

Methods: One hundred and fifty-one participants with normal cognition (n = 76) or mild cognitive impairment (n = 75) were examined in a longitudinal brain aging study at the Memory Centers, University Hospital of Lausanne, Switzerland. Plasma levels of NfL, GFAP, and pTau181 along with CSF biomarkers of AD pathology were measured at baseline. NPS were assessed through the Neuropsychiatric Inventory Questionnaire (NPI-Q), along with the cognitive and functional performance at baseline and follow-up (mean: 20 months). Different regression and ROC analyses were used to address the associations of interest.

Results: None of the three plasma biomarker was associated with NPS at baseline. Higher GFAP levels were associated with the presence of NPS at follow-up (OR = 2.8, p = .002) and both, higher NfL and higher GFAP with an increase in the NPI-Q severity score over time (β = 0.25, p = .034 and β = 0.30, p = .013, respectively). Adding NPS and the plasma biomarkers to a reference model improved the prediction of future NPS (AUC 0.72 to 0.88, p = .002) and AD pathology (AUC 0.78 to 0.87, p = .010), but not of cognitive decline (AUC 0.79 to 0.85, p = .081).

Conclusion: Plasma NfL and GFAP are both associated with future NPS and NPS severity change. Considering the presence of NPS along with blood-based AD-biomarkers may improve the prediction of clinical progression of NPS over time and inform clinical decision-making in non-demented older people.

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血浆神经丝蛋白、胶质纤维酸蛋白和磷酸化 tau 181 作为神经精神症状和相关临床疾病进展的生物标记物。
背景:神经精神症状(NPS)在老年人中很常见,可能出现在痴呆症发展的早期,并且与认知能力的加速衰退有关。在此,我们的目的是研究神经丝蛋白轻链(NfL)、胶质纤维酸蛋白(GFAP)和苏氨酸181磷酸化的tau(pTau181)的血浆水平是否与非痴呆老年人当前的NPS相关,并预测其未来的NPS。此外,我们还测试了NPS与血浆生物标志物的结合是否有助于预测阿尔茨海默病(AD)的病理和认知能力下降:瑞士洛桑大学医院记忆中心对 151 名认知正常(76 人)或轻度认知障碍(75 人)的参与者进行了脑老化纵向研究。研究人员在基线时测量了血浆中的NfL、GFAP和pTau181水平,以及脑脊液中的AD病理生物标志物。通过神经精神量表问卷(NPI-Q)对NPS进行评估,同时评估基线和随访(平均:20个月)时的认知和功能表现。采用不同的回归分析和ROC分析来解决相关问题:结果:三种血浆生物标志物均与基线时的 NPS 无关。较高的 GFAP 水平与随访时 NPS 的存在相关(OR = 2.8,p = .002),较高的 NfL 和较高的 GFAP 水平与 NPI-Q 严重程度评分随时间推移的增加相关(分别为 β = 0.25,p = .034 和 β = 0.30,p = .013)。将NPS和血浆生物标志物加入参考模型可提高对未来NPS(AUC 0.72至0.88,p = .002)和AD病理(AUC 0.78至0.87,p = .010)的预测,但不能提高对认知能力下降(AUC 0.79至0.85,p = .081)的预测:结论:血浆NfL和GFAP均与未来的NPS和NPS严重程度变化有关。结论:血浆 NfL 和 GFAP 都与未来 NPS 和 NPS 严重程度的变化有关。将 NPS 的存在与基于血液的注意力缺失症生物标志物结合起来考虑,可以改善对 NPS 随时间推移的临床进展的预测,并为非痴呆老年人的临床决策提供参考。
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来源期刊
Alzheimer's Research & Therapy
Alzheimer's Research & Therapy 医学-神经病学
CiteScore
13.10
自引率
3.30%
发文量
172
审稿时长
>12 weeks
期刊介绍: Alzheimer's Research & Therapy is an international peer-reviewed journal that focuses on translational research into Alzheimer's disease and other neurodegenerative diseases. It publishes open-access basic research, clinical trials, drug discovery and development studies, and epidemiologic studies. The journal also includes reviews, viewpoints, commentaries, debates, and reports. All articles published in Alzheimer's Research & Therapy are included in several reputable databases such as CAS, Current contents, DOAJ, Embase, Journal Citation Reports/Science Edition, MEDLINE, PubMed, PubMed Central, Science Citation Index Expanded (Web of Science) and Scopus.
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