Cortical laminar binding of PET amyloid and tau tracers in Alzheimer disease

Yi Li, Wai Tsui, Henry Rusinek, Tracy Butler, Lisa Mosconi, Elizabeth Pirraglia, David Mozley, Shankar Vallabhajosula, Ryuichi Harada, Shozo Furumoto, Katsutoshi Furukawa, Hiroyuki Arai, Yukitsuka Kudo, Nobuyuki Okamura, Mony J. De Leon

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)


Neurofibrillary tau pathology and amyloid β (Aβ) plaques, characteristic lesions of Alzheimer disease (AD), show different neocortical laminar distributions. Neurofibrillary-tangle tau pathology tends to be closer to the gray matter-white matter boundary, whereas Aβ is dispersed throughout the width of the cortical ribbon. Methods: Using PET radiotracers for tau and Aβ lesions, we developed an image analysis tool to measure the distance of tracer-positive voxels from the gray matter-white matter boundary. We studied 5 AD and 5 healthy subjects with both 18F-THK5117 (tau) and 11C-Pittsburgh compound B (Aβ) PET. Results: On average, tau-positive voxels were closer to the white matter than were Aβ-positive voxels. This effect was found for all AD subjects and for all regions, both before and after regionally adjusting for the nonspecific white matter binding of both tracers. The differential laminar pattern was validated through postmortem examination. Conclusion: Within cortical lamina, distance measures may be of value in testing PET tracers for their anatomic selectivity.

Original languageEnglish
Pages (from-to)270-273
Number of pages4
JournalJournal of Nuclear Medicine
Issue number2
Publication statusPublished - 2015 Feb 1


  • Amyloid beta
  • Neocortical binding
  • PET
  • Tau


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