Medical Histories of Control Subjects Influence the Biomarker Potential of Plasma Aβ in Alzheimer’s Disease: a Meta-analysis

• Published in: Journal of molecular neuroscience Vol. 70; no. 6; pp. 861 - 870
• Main Authors: Zhang, Shuai, Huang, Si-Yu, An, Xiao-Bin, Zeng, Lu, Ai, Jing
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.06.2020; Springer Nature B.V
• Subjects: Alzheimer Disease - blood; Alzheimer Disease - diagnosis; Alzheimer's disease; Amyloid beta-Peptides - blood; Biomarkers; Biomarkers - blood; Biomedical and Life Sciences; Biomedicine; Cell Biology; Confidence intervals; Heterogeneity; Humans; Medical History Taking - statistics & numerical data; Meta-analysis; Neurochemistry; Neurodegenerative diseases; Neurology; Neurosciences; Peptide Fragments - blood; Plasma; Proteomics; Statistical analysis; Subgroups; Systematic review; Biomarker; Alzheimer’s disease (AD); Amyloid-β; Meta-analysis
• ISSN: 0895-8696; 1559-1166; 1559-1166
• DOI: 10.1007/s12031-020-01510-1

Whether blood amyloid-β (Aβ) could be a peripheral biomarker of Alzheimer’s disease (AD) remains in dispute. In the present study, we conducted a meta-analysis with 19 citations searched from Embase, PubMed, and the Cochrane Library database. Weighted mean difference (WMD) with 95% confidence intervals (CIs) was used to estimate the effect size. We firstly analyzed the plasma Aβ 40 , Aβ 42 , and Aβ 42 /Aβ 40 ratio in AD and control group subjects. However, only a lower level of plasma Aβ 42 was figured out in AD group subjects with weak statistical significance (WMD 1.82; 95% CI 0.59, 3.06; P  = 0.004; I 2  = 84%). We considered that the medical histories of control subjects could influence the biomarker ability of plasma Aβ. Therefore, subgroup analyses were then carried out based on a new recruiting criterion for control subjects, defining as no afflictions of any Aβ-related diseases. Surprisingly, AD group subjects showed a significant decrease in plasma Aβ 42 /Aβ 40 ratio with low heterogeneity among studies (WMD 0.02; 95% CI 0.02, 0.02; P  < 0.00001; I 2  = 0%). Moreover, not only the Aβ 42 /Aβ 40 ratio but also Aβ 42 and Aβ 40 were indifferent between AD and pseudo-control subjects which might be afflicted with Aβ-related diseases. This meta-analysis demonstrated that medical histories of control subjects were interference factors impeding plasma Aβ to be a biomarker of AD.