Changes in plasma biomarkers differentiate clinical stages of Alzheimer's disease using immunomagnetic reduction assays

• Published in: Journal of Alzheimer's disease Vol. 102; no. 2; p. 459
• Main Authors: Chao, Shu-Ping, Lin, Wei-Che, Lu, Cheng-Hsien, Wu, Hsiu-Chuan, Liu, Hsing-Cheng, Hu, Chaur-Jong
• Format: Journal Article
• Language: English
• Published: United States 01.11.2024
• Subjects: Aged; Alzheimer Disease - blood; Alzheimer Disease - diagnosis; Amyloid beta-Peptides - blood; Biomarkers - blood; Cognitive Dysfunction - blood; Cognitive Dysfunction - diagnosis; Female; Humans; Immunomagnetic Separation; Male; Peptide Fragments - blood; tau Proteins - blood; amyloid; immunomagnetic reduction; plasma biomarkers; Alzheimer's disease dementia; amnestic mild cognitive impairment; Alzheimer's disease; tau protein
• ISSN: 1875-8908
• DOI: 10.3233/JAD-240690

Many groups have been using immunomagnetic reduction (IMR) for assaying plasma amyloid-β 1-40 (Aβ ) peptide, Aβ peptide and total tau protein (T-Tau) in cognitively normal controls (NC), patients with amnestic mild cognitive impairment (aMCI) and Alzheimer's disease dementia (ADD). Tremendous results have been independently reported. We used traditional knowledge databases (e.g., PubMed, Embase), papers published at international conferences, and private communications to obtain data involving the use of IMR assay for plasma biomarkers of plasma Aβ , Aβ , and T-Tau in NC, aMCI, and ADD. Results of thirty studies were analyzed, including twenty-five studies published in papers, two studies presented at conferences and three unpublished studies. Among the thirty studies, there were 1189 subjects of NC, 544 aMCI patients and 853 ADD patients. The average value of plasma Aβ in subjects significantly decreased from NC (59.72 pg/ml) to aMCI (45.92 pg/ml, < 0.0001), which was no significant different from ADD (48.34 pg/ml, > 0.05). The average level of plasma Aβ significantly increased from NC (15.72 pg/ml) to aMCI (17.66 pg/ml, < 0.0001), which was not significantly different from ADD (19.39 pg/ml, > 0.05). However, the average level of plasma T-Tau significantly increased from NC (17.92 pg/ml) to aMCI (28.26 pg/ml, < 0.0001), further significantly increased to AD (35.51 pg/ml, < 0.001). Plasma Aβ , Aβ , and T-Tau levels are able to discriminate NC from patients with aMCI and ADD. Plasma T-Tau levels are disease-severity dependent.