Randomized trial reveals that cerebellar inflammation and metabolism drive cognitive decline in temporal lobe epilepsy, suggesting new treatment strategies.
Key Points
This research aims to understand how cerebellar microglial activation affects glucose metabolism and drives disease progression in temporal lobe epilepsy.
Integrated [18F]FDG PET analysis from 55 patients and a rat model of TLE.
Performed longitudinal [18F]FDG and [18F]DPA-714 microPET/CT imaging to assess metabolism and activation.
Conducted mRNA sequencing and identified c-Fos as a central MAPK signaling regulator.
Patients with TLE showed bilateral cerebellar hypermetabolism.
Rats exhibited increased glucose uptake, Purkinje cell loss, and elevated levels of proinflammatory cytokines.
Pharmacological intervention normalized cerebellar PET signals, reduced seizures, and improved memory performance.