Journal
BRAIN BEHAVIOR AND IMMUNITY
Volume 40, Issue -, Pages 219-225Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2014.03.016
Keywords
Bipolar disorder; Neuroinflammation; Microglia; PET
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Funding
- [EU-FP7-HEALTH-F2-2008-222963]
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Background: The monocyte-T-cell theory of mood disorders regards neuroinflammation, i.e. marked activation of microglia, as a driving force in bipolar disorder. Microglia activation can be visualized in vivo using [C-11]-(R)-PK11195 PET. Indirect evidence suggests the hippocampus as a potential focus of neuroinflammation in bipolar disorder. We aim to determine if there is increased [C-11]-(R)-PK11195binding to activated microglia in the hippocampus of patients with bipolar I disorder when compared to healthy controls. Material and methods: Fourteen patients with bipolar I disorder and eleven healthy controls were included in the analyses. Dynamic 60-min PET scans were acquired after the injection of [C-11]-(R)-PK11195. All subjects underwent psychiatric interviews as well as an MRI scan, which was used for anatomic co-registration in the data analysis. The data from the PET scans was analyzed with a twotissue-compartment model to calculate the binding potential, using the metabolite-corrected plasma and blood curve as input. : A significantly increased [C-11]-(R)-PK11195 binding potential, which is indicative of neuroinflammation, was found in the right hippocampus of the patients when compared to the healthy controls (1.66 (CI 1.45-1.91) versus 1.33 (Cl 1.16-1.53); p = 0.033, respectively). Although the same trend was observed in the left hippocampus, this difference was not statistically significant. Conclusion: This study is the first to demonstrate the presence of focal neuroinflammation in the right hippocampus in bipolar I disorder. (C) 2014 Elsevier Inc. All rights reserved.
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