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Alzheimers Dement (Amst). 2019 Feb 22;11:180-190. doi: 10.1016/j.dadm.2018.12.008. eCollection 2019 Dec.

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

Author information

1
Banner Alzheimer's Institute, Phoenix, AZ, USA.
2
Department of Radiology, Washington University School of Medicine, Saint Louis, MO, USA.
3
Knight Alzheimer Disease Research Center, Washington University School of Medicine, Saint Louis, MO, USA.
4
Division of Biostatistics, Washington University School of Medicine, Saint Louis, MO, USA.
5
Department of Neurological Surgery, University of California, San Francisco, CA, USA.
6
Department of Radiology, University of Michigan, Ann Arbor, MI, USA.
7
Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA.
8
Department of Radiology, Mayo Clinic, Rochester, MN, USA.
9
Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, USA.
10
Butler Hospital, Providence, RI, USA.
11
Department of Neurology, Washington University School of Medicine, Saint Louis, MO, USA.
12
Department of Neurology, University of Pittsburgh, Pittsburgh, PA, USA.
13
Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, USA.
14
University of Puerto Rico, San Juan, Puerto Rico.
15
Yale University School of Medicine, New Haven, CT, USA.
16
University of California-San Diego, San Diego, CA, USA.
17
University of Washington, Seattle, WA, USA.
18
Columbia University, New York, NY, USA.
19
McGill Center for Studies in Aging, Douglas Mental Health Research Institute, Montreal, Canada.
20
University of British Columbia, Vancouver, British Columbia, Canada.
21
Sunnybrook Health Sciences Center, Toronto, Ontario, Canada.
22
The University of New South Wales, Sydney, NSW, Australia.
23
University of Sydney and Royal Prince Alfred Hospital, Sydney, NSW, Australia.
24
University of Western Australia, Crawley, WA, Australia.
25
The University of Melbourne and the Florey Institute, Parkville, VIC, Australia.
26
Inserm U1245, Department of Neurology and CNR-MAJ, Rouen, France.
27
Normandy Center for Genomic and Personalized Medicine, Rouen, France.
28
University Salpêtrière Hospital in Paris, Paris, France.
29
University of Toulouse, Toulouse, France.
30
Hospital Clínic, Barcelona, Spain.
31
University College London, London, UK.
32
Keck School of Medicine at the University of Southern California, Los Angeles, CA, USA.
33
Service Hospitalier Frédéric Joliot, CEA, Orsay, France.
34
F. Hoffmann-La Roche Ltd., Switzerland.

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.

KEYWORDS:

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

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