TY - JOUR
T1 - Comparison of Pittsburgh compound B and florbetapir in cross-sectional and longitudinal studies
AU - Su, Yi
AU - Flores, Shaney
AU - Wang, Guoqiao
AU - Hornbeck, Russ C.
AU - Speidel, Benjamin
AU - Joseph-Mathurin, Nelly
AU - Vlassenko, Andrei G.
AU - Gordon, Brian A.
AU - Koeppe, Robert A.
AU - Klunk, William E.
AU - Jack, Clifford R.
AU - Farlow, Martin R.
AU - Salloway, Stephen
AU - Snider, Barbara J.
AU - Berman, Sarah B.
AU - Roberson, Erik D.
AU - Brosch, Jared
AU - Jimenez-Velazques, Ivonne
AU - van Dyck, Christopher H.
AU - Galasko, Douglas
AU - Yuan, Shauna H.
AU - Jayadev, Suman
AU - Honig, Lawrence S.
AU - Gauthier, Serge
AU - Hsiung, Ging Yuek R.
AU - Masellis, Mario
AU - Brooks, William S.
AU - Fulham, Michael
AU - Clarnette, Roger
AU - Masters, Colin L.
AU - Wallon, David
AU - Hannequin, Didier
AU - Dubois, Bruno
AU - Pariente, Jeremie
AU - Sanchez-Valle, Raquel
AU - Mummery, Catherine
AU - Ringman, John M.
AU - Bottlaender, Michel
AU - Klein, Gregory
AU - Milosavljevic-Ristic, Smiljana
AU - McDade, Eric
AU - Xiong, Chengjie
AU - Morris, John C.
AU - Bateman, Randall J.
AU - Benzinger, Tammie L.S.
N1 - Funding Information:
This research was supported by National Institute of Health grants: P50AG005681, P01AG003991, P01AG026276, U01AG042791, R01AG046179, P30NS048056 R01AG055444, and R01AG031581. Image acquisition and analysis received additional support by UL1TR000448, P30NS098577, and R01EB009352. Research was also supported by BrightFocus Foundation grants A2017272S and A2017330S, Alzheimer's Association Research grant AARG-17-532945, Arizona Alzheimer's Research Consortium, the Charles and Joanne Knight Alzheimer Disease Research Center Support Fund, the David and Betty Farrell Medical Research Fund, the Daniel J. Brennan Alzheimer Research Fund, the Fred Simmons and Olga Mohan Alzheimer Research Support Fund, the Barnes-Jewish Hospital Foundation, the Alzheimer's Association, Eli Lilly and Company, Hoffman La-Roche, Avid Radiopharmaceuticals, GHR Foundation, and an anonymous organization. The authors acknowledge the altruism of the participants and their families and contributions of the DIAN-TU research and support staff at the coordinating center and each of the participating sites for their contributions to this study.
Funding Information:
This research was supported by National Institute of Health grants: P50AG005681 , P01AG003991 , P01AG026276 , U01AG042791 , R01AG046179 , P30NS048056 R01AG055444 , and R01AG031581 . Image acquisition and analysis received additional support by UL1TR000448, P30NS098577, and R01EB009352. Research was also supported by BrightFocus Foundation grants A2017272S and A2017330S , Alzheimer's Association Research grant AARG-17-532945 , Arizona Alzheimer's Research Consortium , the Charles and Joanne Knight Alzheimer Disease Research Center Support Fund, the David and Betty Farrell Medical Research Fund, the Daniel J. Brennan Alzheimer Research Fund, the Fred Simmons and Olga Mohan Alzheimer Research Support Fund, the Barnes-Jewish Hospital Foundation , the Alzheimer's Association , Eli Lilly and Company , Hoffman La-Roche , Avid Radiopharmaceuticals , GHR Foundation , and an anonymous organization. The authors acknowledge the altruism of the participants and their families and contributions of the DIAN-TU research and support staff at the coordinating center and each of the participating sites for their contributions to this study.
Publisher Copyright:
© 2019 [Author/Employing Institution]
PY - 2019/12
Y1 - 2019/12
N2 - Introduction: Quantitative in vivo measurement of brain amyloid burden is important for both research and clinical purposes. However, the existence of multiple imaging tracers presents challenges to the interpretation of such measurements. This study presents a direct comparison of Pittsburgh compound B–based and florbetapir-based amyloid imaging in the same participants from two independent cohorts using a crossover design. Methods: Pittsburgh compound B and florbetapir amyloid PET imaging data from three different cohorts were analyzed using previously established pipelines to obtain global amyloid burden measurements. These measurements were converted to the Centiloid scale to allow fair comparison between the two tracers. The mean and inter-individual variability of the two tracers were compared using multivariate linear models both cross-sectionally and longitudinally. Results: Global amyloid burden measured using the two tracers were strongly correlated in both cohorts. However, higher variability was observed when florbetapir was used as the imaging tracer. The variability may be partially caused by white matter signal as partial volume correction reduces the variability and improves the correlations between the two tracers. Amyloid burden measured using both tracers was found to be in association with clinical and psychometric measurements. Longitudinal comparison of the two tracers was also performed in similar but separate cohorts whose baseline amyloid load was considered elevated (i.e., amyloid positive). No significant difference was detected in the average annualized rate of change measurements made with these two tracers. Discussion: Although the amyloid burden measurements were quite similar using these two tracers as expected, difference was observable even after conversion into the Centiloid scale. Further investigation is warranted to identify optimal strategies to harmonize amyloid imaging data acquired using different tracers.
AB - Introduction: Quantitative in vivo measurement of brain amyloid burden is important for both research and clinical purposes. However, the existence of multiple imaging tracers presents challenges to the interpretation of such measurements. This study presents a direct comparison of Pittsburgh compound B–based and florbetapir-based amyloid imaging in the same participants from two independent cohorts using a crossover design. Methods: Pittsburgh compound B and florbetapir amyloid PET imaging data from three different cohorts were analyzed using previously established pipelines to obtain global amyloid burden measurements. These measurements were converted to the Centiloid scale to allow fair comparison between the two tracers. The mean and inter-individual variability of the two tracers were compared using multivariate linear models both cross-sectionally and longitudinally. Results: Global amyloid burden measured using the two tracers were strongly correlated in both cohorts. However, higher variability was observed when florbetapir was used as the imaging tracer. The variability may be partially caused by white matter signal as partial volume correction reduces the variability and improves the correlations between the two tracers. Amyloid burden measured using both tracers was found to be in association with clinical and psychometric measurements. Longitudinal comparison of the two tracers was also performed in similar but separate cohorts whose baseline amyloid load was considered elevated (i.e., amyloid positive). No significant difference was detected in the average annualized rate of change measurements made with these two tracers. Discussion: Although the amyloid burden measurements were quite similar using these two tracers as expected, difference was observable even after conversion into the Centiloid scale. Further investigation is warranted to identify optimal strategies to harmonize amyloid imaging data acquired using different tracers.
KW - Amyloid imaging
KW - Centiloid
KW - Florbetapir
KW - PiB
KW - Positron emission tomography
UR - http://www.scopus.com/inward/record.url?scp=85061783606&partnerID=8YFLogxK
U2 - 10.1016/j.dadm.2018.12.008
DO - 10.1016/j.dadm.2018.12.008
M3 - Article
C2 - 30847382
AN - SCOPUS:85061783606
SN - 2352-8729
VL - 11
SP - 180
EP - 190
JO - Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
JF - Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
ER -