Neuroinflammation Appears Early on PET Imaging and Then Plateaus in a Mouse Model of Alzheimer Disease

FR Lopez-Picon, A Snellman, O Eskola, S Helin, Olof Solin, M Haaparanta-Solin, JO Rinne

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Neuroinflammation has been associated with various neurologic diseases, including Alzheimer disease (AD). In AD, the translocator protein 18 kDa (TSPO) is overexpressed in the activated microglia that surround the beta-amyloid plaques. In the current longitudinal study using a mouse model of AD, we evaluated the association between beta-amyloid deposition and neuroinflammation in AD. Methods: To monitor the longitudinal changes in b-amyloid deposition and neuroinflammation, we used in vivo PET imaging and ex vivo autoradiography with Pittsburgh compound B (C-11-PIB) and a TSPO tracer, flutriciclamide (F-18-GE-180), in the APP23 mouse model of AD. We also applied immunohistochemistry to study beta-amyloid and activated microglia in the mouse brain tissue. Results: From 17 to 26 mo of age, the mice showed robust increased binding of C-11-PIB with aging in the frontal cortex, parietotemporal cortex, hippocampus, and thalamus whereas the increase in F-18-GE-180 binding with aging was minimal in areas of early amyloidosis such as the frontal cortex and hippocampus. A clear positive correlation between beta-amyloid deposition and neuroinflammation was detected with C-11-PIB and F-18-GE-180 only in the parietotemporal cortex and thalamus. Conclusion: The neuroinflammation increase detected with F-18-GE-180 is less than the increase in amyloidosis detected with C-11-PIB. Furthermore, binding of F-18-GE-180 plateaus at an earlier stage of pathogenesis whereas amyloidosis continues to increase. We suggest that TSPO can be a good marker for early pathogenesis detection but not for tracking long-term disease progression.
Original languageUndefined/Unknown
Pages (from-to)509–515
Number of pages7
JournalJournal of Nuclear Medicine
Issue number3
Publication statusPublished - 2018
MoE publication typeA1 Journal article-refereed


  • GE-180
  • PIB
  • Alzheimer disease
  • beta-amyloid
  • Neuroinflammation

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