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Article type: Research Article
Authors: Cheng, Yuana; c; 1 | Jian, Jie-Minga; c; 1 | He, Chen-Yanga; c | Ren, Jun-Ronga; c | Xu, Man-Yua; c | Jin, Wang-Shenga; c | Tan, Cheng-Ronga; c | Zeng, Gui-Huaa; c | Shen, Ying-Yinga; c | Chen, Dong-Wana; c | Li, Hui-Yuna; c | Yi, Xua; c | Zhang, Yuana; c | Zeng, Fana; c; * | Wang, Yan-Jianga; b; c; d; *
Affiliations: [a] Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China | [b] Institute of Brain and Intelligence, Third Military Medical University, Chongqing, China | [c] Chongqing Key Laboratory of Ageing and Brain Diseases, Chongqing, China | [d] Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China
Correspondence: [*] Correspondence to:Yan-Jiang Wang and Fan Zeng, Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China. E-mails: yanjiang_wang@tmmu.edu.cn and zengfan326@163.com.
Note: [1] These authors contributed equally to this work.
Abstract: Background: The dysregulation of lipid metabolism plays an important role in the pathogenesis of Alzheimer’s disease (AD). Liver-type fatty acid-binding protein (L-FABP, also known as FABP1) is critical for fatty acid transport and may be involved in AD. Objective: To investigate whether the FABP1 level is altered in patients with AD, and its associations with levels of amyloid-β (Aβ) and tau in the plasma and cerebrospinal fluid (CSF). Methods: A cross-sectional study was conducted in a Chinese cohort consisting of 39 cognitively normal controls and 47 patients with AD. The levels of FABP1 in plasma, and Aβ and tau in CSF, were measured by enzyme-linked immunosorbent assay (ELISA). A single-molecule array (SIMOA) was used to detect plasma Aβ levels. Results: The level of plasma FABP1 was significantly elevated in the AD group (p = 0.0109). Further analysis showed a positive correlation of FABP1 with CSF total tau (t-tau) and phosphorylated tau (p-tau) levels. Besides, plasma FABP1/Aβ42 (AUC = 0.6794, p = 0.0071) and FABP1/t-tau (AUC = 0.7168, p = 0.0011) showed fair diagnostic efficacy for AD. When combined with other common AD biomarkers including plasma Aβ42, Aβ40, and t-tau, both FABP1/Aβ42 and FABP1/t-tau showed better diagnostic efficacy than using these biomarkers alone. Among all AUC analyses, the combination of plasma FABP1/t-tau and Aβ42 had the highest diagnostic value (AUC = 0.8075, p < 0.0001). Conclusion: These findings indicate that FABP1 may play a role in AD pathogenesis and be worthy of further investigation in the future.
Keywords: Alzheimer’s disease, amyloid-β, liver-type fatty acid-binding protein, tau
DOI: 10.3233/JAD-220126
Journal: Journal of Alzheimer's Disease, vol. 88, no. 1, pp. 375-383, 2022
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