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J Alzheimers Dis. 2018;62(4):1691-1702. doi: 10.3233/JAD-170840.

18F-Flortaucipir Binding in Choroid Plexus: Related to Race and Hippocampus Signal.

Lee CM1,2, Jacobs HIL1,2,3,4, Marquié M5,6, Becker JA1,2, Andrea NV1,2, Jin DS1,2, Schultz AP2,7, Frosch MP5,6,8,3, Gómez-Isla T5,6,3, Sperling RA5,7,9,3, Johnson KA1,2,5,9,3.

Author information

1
Division of Nuclear Medicine and Molecular Imaging, Massachusetts General Hospital, Boston, MA, USA.
2
Department of Radiology, Massachusetts General Hospital, Boston, MA, USA.
3
Harvard Medical School, Boston, MA, USA.
4
School for Mental Health and Neuroscience, Faculty of Health, Medicine and Life Sciences, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
5
Department of Neurology, Massachusetts General Hospital, Boston, MA, USA.
6
MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Boston, MA, USA.
7
The Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Boston, MA, USA.
8
C.S. Kubik Laboratory for Neuropathology, Massachusetts General Hospital, Boston, MA, USA.
9
Department of Neurology, Center for Alzheimer Research and Treatment, Brigham and Women's Hospital, Boston, MA, USA.

Abstract

BACKGROUND:

On target 18F-Flortaucipir (FTP) binding of Alzheimer's disease tau aggregates and off-target binding of melanocytes have been demonstrated with autoradiography.

OBJECTIVE:

We aimed to investigate the hypothesis that if binding in choroid plexus (CP) is due to melanocytes, the signal would be elevated in Black/African American (B/AA) compared to White (W) participants. In addition, we examined whether CP signal affects measurements in adjacent regions, and whether correcting for spill-in effects has an influence on associations between hippocampus (HC) FTP and amyloid or cognition.

METHODS:

FTP race differences in 147 Harvard Aging Brain Study participants (23 B/AA, 124W) were examined in CP, HC, HC covaried for CP, amygdala, inferior temporal gyrus, entorhinal cortex, and fusiform regions. Associations between CP FTP and other regions-of-interest (ROIs) were probed to assess spill-in effects. A statistical regression approach to attenuate CP spill-in was tested by relating adjusted HC SUVR residuals and unadjusted HC SUVR to race, cognition and amyloid. All analyses were covaried for age, sex, education and amyloid deposition, and Bonferroni-corrected for multiple comparisons.

RESULTS:

B/AA individuals had elevated CP and HC SUVR (p < 0.007), whereas other ROI SUVR and HC SUVR covaried for CP SUVR did not show race differences (p > 0.05). CP SUVR was associated with HC SUVR (p < 10-14), but with no other ROI SUVR (p > 0.05). When adjusting HC SUVR for CP SUVR, no race differences in residual HC SUVR were detected, and relationships with amyloid and memory became apparent.

CONCLUSION:

Melanocyte FTP binding may account partially for high CP signal. This off-target binding affects mainly HC FTP measurements, which should be interpreted with caution.

KEYWORDS:

Alzheimer’s disease; choroid plexus; melanin; off-target binding; race; tau PET

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