Data_Sheet_1_Association of Circulating Apolipoprotein AI Levels in Patients With Alzheimer's Disease: A Systematic Review and Meta-Analysis.xlsx

With the development of medicine, our research on Alzheimer's disease (AD) has been further deepened, but the mechanism of its occurrence and development has not been fully revealed, and there is currently no effective treatment method. Several studies have shown that apolipoprotein AI (ApoA-I) can affect the occurrence and development of Alzheimer's disease by binding to amyloid β (Aβ). However, the association between circulating levels of ApoA-I and AD remains controversial. We conducted a meta-analysis of 18 studies published between 1992 and 2017 to determine whether the ApoA-I levels in the blood and cerebrospinal fluid (CSF) are abnormal in AD. Literatures were searched in PubMed, EMBASE and Web of Science databases without language limitations. A pooled subject sample including 1,077 AD patients and 1,271 healthy controls (HCs) was available to assess circulating ApoA-I levels; 747 AD patients and 680 HCs were included for ApoA-I levels in serum; 246 AD patients and 456 HCs were included for ApoA-I levels in plasma; 201 AD patients and 447 HCs were included for ApoA-I levels in CSF. It was found that serum and plasma levels of ApoA-I were significantly reduced in AD patients compared with HCs {[standardized mean difference (SMD) = −1.16; 95% confidence interval (CI) (−1.72, −0.59); P = 0.000] and [SMD = −1.13; 95% CI (−2.05, −0.21); P = 0.016]}. Patients with AD showed a tendency toward higher CSF ApoA-I levels compared with HCs, although this difference was non-significant [SMD = 0.20; 95% CI (−0.16, 0.56); P = 0.273]. In addition, when we analyzed the ApoA-I levels of serum and plasma together, the circulating ApoA-I levels in AD patients was significantly lower [SMD = −1.15; 95% CI (−1.63, −0.66); P = 0.000]. These results indicate that ApoA-I deficiency may be a risk factor of AD, and ApoA-I has the potential to serve as a biomarker for AD and provide experimental evidence for diagnosis of AD.
Systematic Review Registration: PROSPERO, identifier: 325961.

随着医学的发展，我们对阿尔茨海默病（Alzheimer's disease, AD）的研究进一步深入，但其发生发展的机制尚未完全阐明，目前尚无有效的治疗手段。多项研究表明，载脂蛋白AI（apolipoprotein AI, ApoA-I）可通过结合淀粉样β蛋白（amyloid β, Aβ）影响阿尔茨海默病的发生发展，但循环中载脂蛋白AI水平与阿尔茨海默病的关联仍存在争议。本研究对1992年至2017年间发表的18项研究进行了荟萃分析，旨在探讨阿尔茨海默病患者血液与脑脊液（cerebrospinal fluid, CSF）中载脂蛋白AI水平是否存在异常。研究未设置语言限制，在PubMed、EMBASE及Web of Science数据库中检索相关文献。合并的受试者样本包含1077例阿尔茨海默病患者与1271例健康对照（healthy controls, HCs），用于评估循环载脂蛋白AI水平；其中针对血清载脂蛋白AI水平的分析纳入747例阿尔茨海默病患者与680例健康对照，针对血浆载脂蛋白AI水平的分析纳入246例阿尔茨海默病患者与456例健康对照，针对脑脊液载脂蛋白AI水平的分析纳入201例阿尔茨海默病患者与447例健康对照。研究发现，与健康对照相比，阿尔茨海默病患者的血清与血浆载脂蛋白AI水平显著降低[标准化均数差（standardized mean difference, SMD）=-1.16；95%置信区间（confidence interval, CI）(-1.72, -0.59)；P=0.000]以及[SMD=-1.13；95%CI(-2.05, -0.21)；P=0.016]。阿尔茨海默病患者的脑脊液载脂蛋白AI水平较健康对照呈升高趋势，但该差异无统计学意义[SMD=0.20；95%CI(-0.16, 0.56)；P=0.273]。此外，当合并分析血清与血浆中的载脂蛋白AI水平时，阿尔茨海默病患者的循环载脂蛋白AI水平显著降低[SMD=-1.15；95%CI(-1.63, -0.66)；P=0.000]。上述结果提示，载脂蛋白AI缺乏可能是阿尔茨海默病的危险因素，载脂蛋白AI有望成为阿尔茨海默病的生物标志物，为阿尔茨海默病的诊断提供实验依据。系统评价注册：PROSPERO，编号：325961。