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

• Published in: Epilepsy research Vol. 137; pp. 69 - 72
• Main Authors: Joutsa, Juho, Rinne, Juha O., Karrasch, Mira, Hermann, Bruce, Johansson, Jarkko, Anttinen, Anu, Eskola, Olli, Helin, Semi, Shinnar, Shlomo, Sillanpää, Matti
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.11.2017
• Subjects: Aging; Alzheimer’s; Amyloid - metabolism; Benzothiazoles; Brain - diagnostic imaging; Brain - metabolism; Brain Mapping; Epilepsy; Epilepsy - diagnostic imaging; Epilepsy - metabolism; Female; Fluorodeoxyglucose F18; Follow-Up Studies; Glucose - metabolism; Humans; Imaging; Male; Middle Aged; Positron emission tomography; Radiopharmaceuticals; Aging; Positron emission tomography; Epilepsy; Imaging; Alzheimer’s
• ISSN: 0920-1211; 1872-6844; 1872-6844
• DOI: 10.1016/j.eplepsyres.2017.09.006

•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.