Tong Jun-Hui, Gong Shi-Qiang, Zhang Yan-Song, Dong Jian-Ru, Zhong Xin, Wei Min-Jie, Liu Ming-Yan
Department of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Front Aging Neurosci. 2022 May 18;14:899175. doi: 10.3389/fnagi.2022.899175. eCollection 2022.
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); = 0.000] and [SMD = -1.13; 95% CI (-2.05, -0.21); = 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); = 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); = 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. PROSPERO, identifier: 325961.
随着医学的发展，我们对阿尔茨海默病（AD）的研究进一步深入，但该病发生和发展的机制尚未完全揭示，目前也没有有效的治疗方法。多项研究表明，载脂蛋白AI（ApoA-I）可通过与β淀粉样蛋白（Aβ）结合来影响阿尔茨海默病的发生和发展。然而，ApoA-I的循环水平与AD之间的关联仍存在争议。我们对1992年至2017年间发表的18项研究进行了荟萃分析，以确定AD患者血液和脑脊液（CSF）中的ApoA-I水平是否异常。在PubMed、EMBASE和Web of Science数据库中检索文献，无语言限制。共有包括1077例AD患者和1271例健康对照（HCs）的汇总样本用于评估循环ApoA-I水平；747例AD患者和680例HCs纳入血清ApoA-I水平分析；246例AD患者和456例HCs纳入血浆ApoA-I水平分析；201例AD患者和447例HCs纳入脑脊液ApoA-I水平分析。结果发现，与HCs相比，AD患者血清和血浆中的ApoA-I水平显著降低{[标准化均数差（SMD）=-1.16；95%置信区间（CI）（-1.72，-0.59）；P = 0.000]和[SMD = -1.13；95% CI（-2.05，-0.21）；P = 0.016]}。与HCs相比，AD患者脑脊液ApoA-I水平有升高趋势，尽管这种差异不显著[SMD = 0.20；95% CI（-0.16，0.56）；P = 0.273]。此外，当我们将血清和血浆中的ApoA-I水平一起分析时，AD患者的循环ApoA-I水平显著降低[SMD = -1.15；95% CI（-1.63，-0.66）；P = 0.000]。这些结果表明，ApoA-I缺乏可能是AD的一个危险因素，ApoA-I有潜力作为AD的生物标志物，为AD的诊断提供实验证据。国际前瞻性系统评价注册库（PROSPERO），标识符：325961。
