| First Author | Barron AM | Year | 2020 |
| Journal | Neurobiol Aging | Volume | 94 |
| Pages | 140-148 | PubMed ID | 32623260 |
| Mgi Jnum | J:298310 | Mgi Id | MGI:6478715 |
| Doi | 10.1016/j.neurobiolaging.2020.05.003 | Citation | Barron AM, et al. (2020) In vivo positron emission tomography imaging of mitochondrial abnormalities in a mouse model of tauopathy. Neurobiol Aging 94:140-148 |
| abstractText | Damaged mitochondria may be one of the earliest manifestations of Alzheimer's disease. Because oxidative phosphorylation is a primary source of neuronal energy, unlike glycolysis-dependent energy production in inflamed glia, mitochondrial respiration could provide a selective biomarker of neuronal deterioration in Alzheimer's disease. Here we used a recently developed positron emission tomography (PET) probe targeting mitochondrial complex I (MC-I), (18)F-BCPP-EF, to non-invasively visualize mitochondrial abnormalities in the brains of tau transgenic mice (rTg4510). Tauopathy and neuroinflammation were visualized by PET using a tau probe (11)C-PBB3 and a translocator protein probe, (18)F-FEBMP, respectively. A marked reduction in (18)F-BCPP-EF uptake was observed in hippocampal and forebrain regions of tau transgenic mice, colocalizing with regions of tauopathy, neuronal damage, and neuroinflammation. MC-I signals were highly correlated with atrophy assayed by magnetic resonance imaging, but negatively associated with inflammatory signals, indicating that neuronal metabolic signals measured by MC-I PET were robust to inflammatory interference. MC-I may be a useful imaging biomarker to detect neuronal damage and metabolic changes with minimal interference from concomitant glial hypermetabolism. |
