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Updated: Apr 28, 2026

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
Published on: September 28, 2019
Comparing amyloid-β deposition, neuroinflammation, glucose metabolism, and mitochondrial complex I activity in brain:
Hideo Tsukada1, Shingo Nishiyama, Hiroyuki Ohba
1Central Research Laboratory, Hamamatsu Photonics K.K., 5000 Hirakuchi, Hamakita, Shizuoka, 434-8601, Japan, tsukada@crl.hpk.co.jp.
Purpose:
The aim of the present study was to compare amyloid-β (Aβ) deposition, translocator protein (TSPO) activity, regional cerebral metabolic rate of glucose (rCMRglc), and mitochondrial complex I (MC-I) activity in the brain of aged monkeys.
Methods:
PET scans with (11)C-PIB (Aβ), (18)F-BCPP-EF (MC-I), (11)C-DPA-713 (TSPO), and (18)F-FDG (rCMRglc) were performed in aged monkeys (Macaca mulatta) in the conscious state and under isoflurane anaesthesia. (11)C-PIB binding to Aβ and (11)C-DPA-713 binding to TSPO were evaluated in terms of standard uptake values (SUV). The total volume of distribution (V T) of (18)F-BCPP-EF and rCMRglc with (18)F-FDG were calculated using arterial blood sampling.
Results:
Isoflurane did not affect MC-I activity measured in terms of (18)F-BCPP-EF uptake in living brain. There was a significant negative correlation between (18)F-BCPP-EF binding (V T) and (11)C-PIB uptake (SUVR), and there was a significant positive correlation between (11)C-DPA-713 uptake (SUV) and (11)C-PIB uptake. In contrast, there was no significant correlation between rCMRglc ratio and (11)C-PIB uptake.
Conclusion:
(18)F-BCPP-EF could be a potential PET probe for quantitative imaging of impaired MC-I activity that is correlated with Aβ deposition in the living brain.
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