Short communicationBrain glucose metabolism and its relation to amyloid load in middle-aged adults with childhood-onset epilepsy

- Childhood-onset epilepsy is associated with increased brain amyloid accumulation.
- It is not known if increased amyloid in epilepsy leads to neurodegeneration.
- Brain glucose metabolism was investigated in adults with childhood-onset epilepsy.
- Brain amyloid load was associated with increased regional metabolism.
- Increased brain metabolism may be an early sign of a neurodegenerative process.

Uncomplicated childhood-onset epilepsy is associated with increased brain amyloid load at late middle age, but its possible association with Alzheimer-type neurodegenerative processes is unclear. After 50-year follow-up, 42 childhood onset epilepsy subjects and 45 matched controls were investigated with [18F]fluorodeoxyglucose PET. There were no significant differences between the subjects and controls, but higher [18F]fluorodeoxyglucose uptake was associated with a higher local amyloid load (as measured with [11C]PIB PET) in the prefrontal cortex, parietal cortex, and posterior cingulate/precuneus in subjects but not in controls. These findings parallel reported observations in cognitively normal individuals with increased brain amyloid accumulation who are at risk for future Alzheimer's disease.