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Plasma Aβ analysis using magnetically-labeled immunoassays and PET 18F-florbetapir binding in non-demented patients with major depressive disorder.

Plasma Aβ analysis using magnetically-labeled immunoassays and PET 18F-florbetapir binding in non-demented patients with major depressive disorder.
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Wu KY, Hsiao IT, Chen CH, Liu CY, Hsu JL, Huang SY, Yen TC, Lin KJ,


Wu KY, Hsiao IT, Chen CH, Liu CY, Hsu JL, Huang SY, Yen TC, Lin KJ, (click to view)

Wu KY, Hsiao IT, Chen CH, Liu CY, Hsu JL, Huang SY, Yen TC, Lin KJ,

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Scientific reports 2018 02 098(1) 2739 doi 10.1038/s41598-018-21140-3
Abstract

An increased level of brain amyloid deposition and a decreased level of cerebral spinal fluid (CSF) Aβ42 are currently considered reliable biomarkers of Alzheimer’s disease (AD); however, the usefulness of plasma Aβ levels are not well-established. This study investigated the relationships between plasma Aβ levels and cerebral amyloidosis in 36 non-demented patients with major depressive disorder (MDD). All participants underwent 18F-florbetapir PET imaging and provided a blood sample at the same time for immunomagnetic reduction assay to measure the plasma levels of Aβ40 and Aβ42. We found inverse associations of the plasma Aβ42 level and the Aβ42/Aβ40 ratio, and a positive association of the plasma Aβ40 level, with cerebral amyloid deposition in the precuneus, parietal and posterior cingulate cortex. Subgroup analyses in subjects with higher 18F-florbetapir uptake values or MDD with amnestic mild cognitive impairment revealed more pervasive relationships of plasma Aβ measures with 18F-florbetapir binding across the brain regions examined. The study suggested that regional brain amyloid deposition in terms of 18F-florbetapir PET uptake had weak-to-moderate associations with plasma Aβ42 and Aβ40 levels, and the Aβ42/Aβ40 ratio. Validation in a larger population of subjects of known cerebral amyloidosis status is needed. Careful interpretation of plasma data is warranted.

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