Comparison of Pittsburgh compound B and florbetapir in cross-sectional and longitudinal studies

Yi Su, Shaney Flores, Guoqiao Wang, Russ C. Hornbeck, Benjamin Speidel, Nelly Joseph-Mathurin, Andrei G. Vlassenko, Brian A. Gordon, Robert A. Koeppe, William E. Klunk, Clifford R. Jack, Martin R. Farlow, Stephen Salloway, Barbara J. Snider, Sarah B. Berman, Erik D. Roberson, Jared Brosch, Ivonne Jimenez-Velazques, Christopher H. van Dyck, Douglas GalaskoShauna H. Yuan, Suman Jayadev, Lawrence S. Honig, Serge Gauthier, Ging Yuek R. Hsiung, Mario Masellis, William S. Brooks, Michael Fulham, Roger Clarnette, Colin L. Masters, David Wallon, Didier Hannequin, Bruno Dubois, Jeremie Pariente, Raquel Sanchez-Valle, Catherine Mummery, John M. Ringman, Michel Bottlaender, Gregory Klein, Smiljana Milosavljevic-Ristic, Eric McDade, Chengjie Xiong, John C. Morris, Randall J. Bateman, Tammie L.S. Benzinger

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)180-190
Number of pages11
JournalAlzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
Volume11
DOIs
StatePublished - Dec 2019

Bibliographical note

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]

Keywords

  • Amyloid imaging
  • Centiloid
  • Florbetapir
  • PiB
  • Positron emission tomography

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