Abstract
Background and Objectives Previous research has demonstrated increased brain amyloid plaque load in individuals with childhood-onset epilepsy in late middle age. However, the trajectory of this process is not yet known. The aim of this study was to determine whether individuals with a history of childhood-onset epilepsy show progressive brain aging in amyloid accumulation in late adulthood (Turku Adult Childhood-Onset Epilepsy study, TACOE). Methods Adults from a prospective population-based cohort of individuals with childhood-onset epilepsy, originally recruited 1961-1964, together with matched controls, were scanned with [ 11C]PIB PET twice: after at least 50 years (TACOE-50) and again after at least 55 years (TACOE-55) from the diagnosis. ResultsAt TACOE-55, 31.4% (11/36, mean age 63.3 years, 52.8% female) of individuals from the epilepsy group and 11.4% (4/35, 63.1 year, 54.3%) of controls had a visually abnormal [ 11C]PIB scan (p = 0.039). At TACOE-55, cortical brain [ 11C]PIB uptakes were higher and increased more from TACOE-50 in the epilepsy compared with the control group (p < 0.05). In voxelwise whole-brain analyses, the epilepsy group showed significantly higher and more widespread brain amyloid accumulation (pFWE < 0.05). Discussion The results demonstrate that childhood-onset epilepsy is associated with an earlier age at onset of amyloidosis and greater progressive amyloid accumulation in late adulthood.
| Original language | English |
|---|---|
| Article number | e210303 |
| Journal | Neurology |
| Volume | 104 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 17 Jan 2025 |
| MoE publication type | A1 Journal article-refereed |
Funding
J. Joutsa has received conference travel support from Insightec, Abbvie, and Abbott; lecturer honoraria from Lundbeck, Novartis, Addiktum, and Nordic Infucare; consultancy fees from Summaryx and Adamant Health; acts as an advisory board member and consultant for Teva Finland; and owns stock of Neurologic Finland and Suomen Neurolaboratorio. J.O. Rinne serves as a neurology consultant for CRST Oy (Clinical Research Services Turku), as a member of a global expert panel for NOVO Nordisk, and as a member of a data monitoring committee for Lundbeck. K.J. Niemi has received conference travel support from the Finnish Parkinson Foundation, the Finnish Neurological Society, the Finnish Society of Nuclear Medicine, the Finnish Cultural Foundation (Pertteli Aaltonen Fund), Turku University Hospital, the University of Turku, and Merck; and has minor stock ownership in CareCloud, GlaxoSmithKline, Modulight, Nightingale Health, and Physicians Realty Trust. M. Karrasch, R.K. Parkkola, J. Saunavaara, B.P. Hermann, and M. Sillanp\u00E4\u00E4 report no disclosures relevant to the manuscript. Go to Neurology.org/N for full disclosures. This work was funded by CURE Epilepsy (Innovator Award, Epilepsy Award, and Epilepsy Research Continuity Fund Award) (B.H., M.S), National Governmental Research Grant (VTR), and Pro Humanitate Foundation, and Sigrid Juselius Foundation. J. Joutsa received funding from the Research Council of Finland, Finnish Medical Foundation, Sigrid Juselius Foundation, Finnish Foundation for Alcohol Studies, University of Turku (private donation), and Turku University Hospital (VTR). J.O. Rinne has received funding from the Academy of Finland (project #310962), Sigrid Juselius Foundation, and Finnish Governmental Research Funding (VTR) for Turku University Hospital.