Swaminathan, Shanker; Risacher, Shannon L; Yoder, Karmen K; West, John D; Shen, Li; Kim, Sungeun; Inlow, Mark; Foroud, Tatiana; Jagust, William J; Koeppe, Robert A; Mathis, Chester A; Shaw, Leslie M; Trojanowski, John Q; Soares, Holly; Aisen, Paul S; Petersen, Ronald C; Weiner, Michael W; Saykin, Andrew J; Initiative, Alzheimer's Disease Neuroimaging

doi:10.1016/j.jalz.2013.01.007

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Association of plasma and cortical amyloid beta is modulated by APOE ε4 status

Published Web Location

https://doi.org/10.1016/j.jalz.2013.01.007

Abstract

Background

Apolipoprotein E (APOE) ε4 allele's role as a modulator of the relationship between soluble plasma amyloid beta (Aβ) and fibrillar brain Aβ measured by Pittsburgh compound B positron emission tomography ([(11)C]PiB PET) has not been assessed.

Methods

Ninety-six Alzheimer's Disease Neuroimaging Initiative participants with [(11)C]PiB scans and plasma Aβ1-40 and Aβ1-42 measurements at the time of PET scanning were included. Regional and voxelwise analyses of [(11)C]PiB data were used to determine the influence of APOE ε4 allele on association of plasma Aβ1-40, Aβ1-42, and Aβ1-40/Aβ1-42 with [(11)C]PiB uptake.

Results

In APOE ε4- but not ε4+ participants, positive relationships between plasma Aβ1-40/Aβ1-42 and [(11)C]PiB uptake were observed. Modeling the interaction of APOE and plasma Aβ1-40/Aβ1-42 improved the explained variance in [(11)C]PiB binding compared with using APOE and plasma Aβ1-40/Aβ1-42 as separate terms.

Conclusions

The results suggest that plasma Aβ is a potential Alzheimer's disease biomarker and highlight the importance of genetic variation in interpretation of plasma Aβ levels.

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