Investigations of reported plasma amyloid b peptides and total tau protein assayed with immunomagnetic reduction in cognitively normal controls and patients with amnestic mild cognitive impairment and Alzheimer’s disease dementia

Abstract Background Since 2012, many groups have been using immunomagnetic reduction (IMR) for assaying plasma amyloid β 1‐40 (Aβ 1‐40 ) peptide, Aβ 1‐42 peptide and total tau protein (T‐Tau) in cognitively normal controls (NC) and patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease dementia (ADD). Tremendous results have been independently reported. In this work, we summarize the reported levels of plasma Aβ 1‐40 , Aβ 1‐42 and T‐Tau to investigate the consistence among studies. Method Results of thirty studies were analyzed, including twenty‐five studies published in papers, two studies presented at conferences and three unpublished studies. Result The coefficient of variation (CV) in reported mean values of biomarker concentrations among studies are 8.1% for Aβ 1‐40 , 4.1% for Aβ 1‐42 and 19.4% for T‐Tau in NC, 10.7% for Aβ 1‐40 , 8.4% for Aβ 1‐42 and 15.0% for T‐Tau in aMCI, 10.6% for Aβ 1‐40 , 19.1% for Aβ 1‐42 and 28.7% for T‐Tau in ADD. In the thirty studies, there are 1189 subjects of NC, 543 aMCI patients and 853 ADD patients. The averaged level of plasma Aβ 1‐40 of subjects was found to significantly decrease from NC (59.72 pg/ml) to aMCI (45.92 pg/ml, p < 0.0001), which showed non‐significant difference from ADD (48.34 pg/ml, p > 0.05). The averaged level of plasma Aβ 1‐42 significantly increased from NC (15.72 pg/ml) to aMCI (17.66 pg/ml, p < 0.0001), which was not significantly different from ADD (19.39 pg/ml, p > 0.05). However, the averaged level of plasma T‐Tau significantly increased from NC (17.92 pg/ml) to aMCI (28.26 pg/ml, p < 0.0001), further significantly increased to ADD (35.51 pg/ml, p < 0.001). The summarized results reveal important impacts to clinical utilities of plasma biomarkers in AD. Conclusion The measured concentrations of plasma Aβ 1‐40 , Aβ 1‐42 and T‐Tau with IMR are consistent and reliable among studies. Furthermore, the plasma Aβ 1‐40 , Aβ 1‐42 and T‐Tau levels are able to discriminate NC from patients with aMCI and ADD. Plasma T‐Tau levels are disease‐severity dependent.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2024-12-01
DOI
https://doi.org/10.1002/alz.090058
Primary Topic
Alzheimer's disease research and treatments
Type
article
Field-Weighted Citation Impact
0.00
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article

Investigations of reported plasma amyloid b peptides and total tau protein assayed with immunomagnetic reduction in cognitively normal controls and patients with amnestic mild cognitive impairment and Alzheimer’s disease dementia

Caishui Yang
Alzheimer s & Dementia
Alzheimer's disease research and treatments
article

Investigations of reported plasma amyloid b peptides and total tau protein assayed with immunomagnetic reduction in cognitively normal controls and patients with amnestic mild cognitive impairment and Alzheimer’s disease dementia

Caishui Yang
article en

Abstract

Abstract Background Since 2012, many groups have been using immunomagnetic reduction (IMR) for assaying plasma amyloid β 1‐40 (Aβ 1‐40 ) peptide, Aβ 1‐42 peptide and total tau protein (T‐Tau) in cognitively normal controls (NC) and patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease dementia (ADD). Tremendous results have been independently reported. In this work, we summarize the reported levels of plasma Aβ 1‐40 , Aβ 1‐42 and T‐Tau to investigate the consistence among studies. Method Results of thirty studies were analyzed, including twenty‐five studies published in papers, two studies presented at conferences and three unpublished studies. Result The coefficient of variation (CV) in reported mean values of biomarker concentrations among studies are 8.1% for Aβ 1‐40 , 4.1% for Aβ 1‐42 and 19.4% for T‐Tau in NC, 10.7% for Aβ 1‐40 , 8.4% for Aβ 1‐42 and 15.0% for T‐Tau in aMCI, 10.6% for Aβ 1‐40 , 19.1% for Aβ 1‐42 and 28.7% for T‐Tau in ADD. In the thirty studies, there are 1189 subjects of NC, 543 aMCI patients and 853 ADD patients. The averaged level of plasma Aβ 1‐40 of subjects was found to significantly decrease from NC (59.72 pg/ml) to aMCI (45.92 pg/ml, p < 0.0001), which showed non‐significant difference from ADD (48.34 pg/ml, p > 0.05). The averaged level of plasma Aβ 1‐42 significantly increased from NC (15.72 pg/ml) to aMCI (17.66 pg/ml, p < 0.0001), which was not significantly different from ADD (19.39 pg/ml, p > 0.05). However, the averaged level of plasma T‐Tau significantly increased from NC (17.92 pg/ml) to aMCI (28.26 pg/ml, p < 0.0001), further significantly increased to ADD (35.51 pg/ml, p < 0.001). The summarized results reveal important impacts to clinical utilities of plasma biomarkers in AD. Conclusion The measured concentrations of plasma Aβ 1‐40 , Aβ 1‐42 and T‐Tau with IMR are consistent and reliable among studies. Furthermore, the plasma Aβ 1‐40 , Aβ 1‐42 and T‐Tau levels are able to discriminate NC from patients with aMCI and ADD. Plasma T‐Tau levels are disease‐severity dependent.

Alzheimer s & DementiaVol. 20(S2)
Openalex Percentile: Top 65%
Alzheimer's disease research and treatments
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