Swaminathan, ShankerRisacher, Shannon L.Yoder, Karmen K.West, John D.Shen, LiKim, SungeunInlow, MarkForoud, TatianaJagust, William J.Koeppe, Robert A.Mathis, Chester A.Shaw, Leslie M.Trojanowski, John Q.Soares, HollyAisen, Paul S.Petersen, Ronald C.Weiner, Michael W.Saykin, Andrew J.2016-02-182016-02-182014-01Swaminathan, S., Risacher, S. L., Yoder, K. K., West, J. D., Shen, L., Kim, S., … Saykin, A. J. (2014). Association of plasma and cortical beta-amyloid is modulated by APOE ε4 status. Alzheimer’s & Dementia : The Journal of the Alzheimer’s Association, 10(1). http://doi.org/10.1016/j.jalz.2013.01.0071552-5260https://hdl.handle.net/1805/8377Background: APOE ε4’s role as a modulator of the relationship between soluble plasma beta-amyloid (Aβ) and fibrillar brain Aβ measured by Pittsburgh Compound-B positron emission tomography ([11C]PiB PET) has not been assessed. Methods: Ninety-six Alzheimer’s Disease Neuroimaging Initiative participants with [11C]PiB scans and plasma Aβ1-40 and Aβ1-42 measurements at time of scan were included. Regional and voxel-wise analyses of [11C]PiB data were used to determine the influence of APOE ε4 on association of plasma Aβ1-40, Aβ1-42, and Aβ1-40/Aβ1-42 with [11C]PiB uptake. Results: In APOE ε4− but not ε4+ participants, positive relationships between plasma Aβ1-40/Aβ1-42 and [11C]PiB uptake were observed. Modeling the interaction of APOE and plasma Aβ1-40/Aβ1-42 improved the explained variance in [11C]PiB binding compared to 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.en-USPublisher PolicyAlzheimer’s disease (AD)mild cognitive impairment (MCI)Alzheimer’s Disease Neuroimaging Initiative (ADNI)beta-amyloid (A β)plasma beta-amyloidpositron emission tomography (PET)Pittsburgh Compound-B ([11C]PiB)Apolipoprotein E (APOE)