Authors :
Presenting Author: Jing Wang, PhD – Zhongshan Hospital Fudan University
Siwei liu, MD – Zhongshan Hospital Fudan University
Yuchen Gong, PhD – Shanghai Jiao Tong University
Jing Ding, MD，PhD – Zhongshan Hospital Fudan University
Rationale:
Microglial activation is a hallmark feature in the pathogenesis and progression of epilepsy. PET radioligands targeting the 18-kDa translocator protein (TSPO) serve as in vivo markers of neuroinflammation.18F-ER176, a third-generation TSPO-targeted radiotracer, exhibits favorable in vivo stability, affinity, specificity, and insensitivity to TSPO gene polymorphism. This study utilized 18F-ER176 TSPO PET to compare microglial activation across brain regions in different epilepsy subtypes, aiming to elucidate the role of microglial activation in epileptogenesis.
Methods:
Patients with confirmed epilepsy diagnoses were enrolled. Each underwent 18F -ER176 and ¹⁸F-FDG PET-MRI to evaluate microglial activation and cerebral glucose metabolism, respectively. The whole brain was segmented into 90 cerebral and 26 cerebellar regions using the Automated Anatomical Labeling (AAL) template. The mean standardized uptake value ratio (SUVR) intensity for each region was calculated and compared. Data processing was performed in MATLAB R2021b, with TSPO-PET and FDG-PET images co-registered to MNI standard space using SPM12. Region-specific analysis was based on the AAL template in MNI space.
Results:
Thirty-seven epilepsy patients were included: 23 with drug-resistant epilepsy (DRE), 14 with non-drug-resistant epilepsy (non-DRE)；23 with temporal lobe epilepsy (TLE), and 14 with non-temporal lobe epilepsy (non-TLE). DRE patients exhibited significant microglial activation in the temporal lobe, parietal lobe, and thalamus, alongside glucose hypermetabolism in the occipital and parietal lobes. TLE patients demonstrated widespread reduced microglial activation in the frontal and temporal lobes, with significant glucose hypometabolism in bilateral temporal lobes.Conclusions:
Microglial activation may contribute to the pathophysiology of drug-resistant epilepsy. Microglial activation participates in the pathological mechanisms of temporal lobe epilepsy, but it may not remain chronically activated.
Funding:
The study was supported by the National Key R&D Program of China (2022YFC2503802).