Open AccessPlasma pyroglutamate‐modified amyloid beta differentiates amyloid pathology
Author(s) -
Wang PeiNing,
Lin KunJu,
Liu HueiChun,
Andreasson Ulf,
Blennow Kaj,
Zetterberg Henrik,
Yang ShiehYueh
Publication year - 2020
Publication title -
alzheimer's and dementia: diagnosis, assessment and disease monitoring
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.497
H-Index - 37
ISSN - 2352-8729
DOI - 10.1002/dad2.12029
Subject(s) - positron emission tomography , nuclear medicine , medicine , amyloid (mycology) , biomarker , amyloid beta , pathology , chemistry , disease , biochemistry
Pyroglutamate‐modified amyloid β (Aβ pE3 ) could be a biomarker for Aβ plaque pathology in the brain. An ultra‐high‐sensitive assay is needed for detecting Aβ pE3‐40 . Methods Immunomagnetic reduction was used for quantification of Aβ pE3‐40 in plasma from 46 participants. The concentrations of Aβ pE3‐40 of these subjects were compared with 18 F‐florbetapir positron emission tomography (PET) images. Results Aβ pE3‐40 concentration was 44.1 ± 28.2 fg/mL in PET‐ (n = 28) and 91.6 ± 54.6 fg/mL in PET+ (n = 18; P < .05). The cutoff value of Aβ pE3‐40 for discriminating PET‐ from PET+ was 55.5 fg/mL, resulting in a sensitivity of 83.3%, a specificity of 71.4%. The concentration of Aβ pE3‐40 showed a moderate correlation (r = 0.437) with PET standardized uptake value ratio. Discussion We did not enroll pre‐clinical AD subject with normal cognition but Aβ PET+. It would be an important issue to explore the feasibility of using Aβ pE3‐40 for screening pre‐clinical subjects. Conclusion These results reveal the feasibility of detecting Aβ pathology using quantification of a plaque‐derived Aβ molecule in plasma.