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Alzheimers Dement. 2017 Aug;13(8):841-849. doi: 10.1016/j.jalz.2017.06.2266. Epub 2017 Jul 19.

Amyloid β concentrations and stable isotope labeling kinetics of human plasma specific to central nervous system amyloidosis.

Author information

1
Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA.
2
Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA; Department of Neurology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO, USA; Department of Neurology, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA.
3
Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA; Department of Neurology, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA.
4
Department of Radiology, Washington University School of Medicine, St. Louis, MO, USA; Department of Neurology, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA.
5
Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA.
6
Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA; Department of Neurology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO, USA; Department of Neurology, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: batemanr@wustl.edu.

Erratum in

Abstract

INTRODUCTION:

Cerebrospinal fluid analysis and other measurements of amyloidosis, such as amyloid-binding positron emission tomography studies, are limited by cost and availability. There is a need for a more practical amyloid β (Aβ) biomarker for central nervous system amyloid deposition.

METHODS:

We adapted our previously reported stable isotope labeling kinetics protocol to analyze the turnover kinetics and concentrations of Aβ38, Aβ40, and Aβ42 in human plasma.

RESULTS:

Aβ isoforms have a half-life of approximately 3 hours in plasma. Aβ38 demonstrated faster turnover kinetics compared with Aβ40 and Aβ42. Faster fractional turnover of Aβ42 relative to Aβ40 and lower Aβ42 and Aβ42/Aβ40 concentrations in amyloid-positive participants were observed.

DISCUSSION:

Blood plasma Aβ42 shows similar amyloid-associated alterations as we have previously reported in cerebrospinal fluid, suggesting a blood-brain transportation mechanism of Aβ. The stability and sensitivity of plasma Aβ measurements suggest this may be a useful screening test for central nervous system amyloidosis.

KEYWORDS:

Amyloid β; Aβ42; Human; Kinetics; Plasma; Turnover

PMID:
28734653
PMCID:
PMC5567785
DOI:
10.1016/j.jalz.2017.06.2266
[Indexed for MEDLINE]
Free PMC Article

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