Abstracts

Rationale: The positron emission tomography (PET) radioligand for adenosine A1 receptor (A1R) [1-methyl-11C] 8-dicyclopropylmethyl-1-methyl-3-propylxanthine (MPDX) has recently been developed for human brain imaging. In the present study, we evaluated the alteration of the A1R in patients with mesial temporal lobe epilepsy (mTLE) in vivo. Methods: Fourteen patients with mTLE were included in this study. Three PET examinations were sequentially performed to measure A1R binding with 11C-MPDX, glucose metabolism with 18F-fluorodeoxyglucose (FDG), and central benzodiazepine receptor binding with 11C-flumazenil (FMZ), and decreases of 11C-FMZ uptake indicate neuronal loss. epileptoc fpcus side was set and converted in left side in all patients. Results: 11C- MPDX did not depict any lesion with significantly decreased nondisplaceable binding potential (BPND) in comparison to healthy controls in both region of interest (ROI) analysis and SPM statistical analysis. Instead, it showed a significant increase of BPND in the frontal and temporal cortex of focal side (p < 0.05). In 18F-FDG PET, the standardized uptake values (SUVs) ratio to the whole brain were decreased in medial temporal in focus side (p < 0.01). In 11C-FMZ PET, the SUV ratio to the cerebellum was also decreased in medial temporal lobe (p<0.01). The area with significantly increased 11C-MPDX binding did not overlap with the areas of neuronal loss detected by decreased 11C-FMZ binding and did not completely overlap with area of reduced18F-FDG uptake. Conclusions: We obtained the first 11C-MPDX PET images reflecting the A1R BPND in human mTLE brain in vivo. 11C-MPDX depicted increased A1R BPND in the areas surrounding the epileptic foci, whereas 18F-FDG demonstrated reduction throughout the brain. The results suggested that A1R might confer neuroprotective or antiepileptic effects in mTLE. Funding: No funding