11C-PBR28 binding to translocator protein increases with progression of Alzheimer's disease

William C. Kreisl, Chul Hyoung Lyoo, Jeih San Liow, Monica Wei, Joseph Snow, Emily Page, Kimberly J. Jenko, Cheryl L. Morse, Sami S. Zoghbi, Victor W. Pike, R. Scott Turner, Robert B. Innis

Research output: Contribution to journalArticlepeer-review

122 Citations (Scopus)

Abstract

This longitudinal study sought to determine whether the 18 kDa translocator protein (TSPO), a marker of neuroinflammation, increases over time in Alzheimer's disease. Positron emission tomography imaging with the TSPO radioligand 11C-PBR28 was performed at baseline and after a median follow-up of 2.7 years in 14 amyloid-positive patients and 8 amyloid-negative controls. Patients had a greater increase in TSPO binding than controls in inferior parietal lobule, precuneus, occipital cortex, hippocampus, entorhinal cortex, and combined middle and inferior temporal cortex. TSPO binding in temporoparietal regions increased from 3.9% to 6.3% per annum in patients, but ranged from -0.5% to 1% per annum in controls. The change in TSPO binding correlated with cognitive worsening on clinical dementia rating scale-sum of boxes and reduced cortical volume. The annual rate of increased TSPO binding in temporoparietal regions was about 5-fold higher in patients with clinical progression (n = 9) compared with those who did not progress (n = 5). TSPO may serve as a biomarker of Alzheimer's progression and response to anti-inflammatory therapies.

Original languageEnglish
Pages (from-to)53-61
Number of pages9
JournalNeurobiology of Aging
Volume44
DOIs
Publication statusPublished - 2016 Aug 1

Bibliographical note

Publisher Copyright:
© 2016 .

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Ageing
  • Developmental Biology
  • Clinical Neurology
  • Geriatrics and Gerontology

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