Late-onset temporal lobe epilepsy: insights from brain atrophy and Alzheimer’s disease biomarkers

颞叶 癫痫 萎缩 神经科学 医学 阿尔茨海默病 病理 疾病 心理学
作者
Alice Ballerini,Niccolò Biagioli,Chiara Carbone,Annalisa Chiari,Manuela Tondelli,Giulia Vinceti,Roberta Bedin,Marcella Malagoli,Maurilio Genovese,Simona Scolastico,Giada Giovannini,Matteo Pugnaghi,Niccolò Orlandi,Louis Lemieux,Stefano Meletti,Giovanna Zamboni,Anna Elisabetta Vaudano
出处
期刊:Brain [Oxford University Press]
被引量:4
标识
DOI:10.1093/brain/awae207
摘要

Abstract Considering the growing age of the world population, the incidence of epilepsy in older adults is expected to increase significantly. It has been suggested that late-onset temporal lobe epilepsy (LO-TLE) may be neurodegenerative in origin and overlap with Alzheimer’s disease (AD). Herein, we aimed to characterize the pattern of cortical atrophy and CSF biomarkers of AD (total and phosphorylated tau and amyloid-β) in a selected population of LO-TLE of unknown origin. We prospectively enrolled individuals with temporal lobe epilepsy onset after the age of 50 and no cognitive impairment. They underwent a structural MRI scan and CSF biomarkers measurement. Imaging and biomarkers data were compared to three retrospectively collected groups: (i) age-sex-matched healthy controls; (ii) patients with mild cognitive impairment (MCI) and abnormal CSF AD biomarkers (MCI-AD); and (iii) patients with MCI and normal CSF AD biomarkers (MCI-noAD). From a pool of 52 patients, 20 consecutive eligible LO-TLE patients with a mean disease duration of 1.8 years were recruited. As control populations, 25 patients with MCI-AD, 25 patients with MCI-noAD and 25 healthy controls were enrolled. CSF biomarkers returned normal values in LO-TLE, significantly different from patients with MCI due to AD. There were no differences in cortico-subcortical atrophy between epilepsy patients and healthy controls, while patients with MCI demonstrated widespread injuries of cortico-subcortical structures. Individuals with LO-TLE, characterized by short disease duration and normal CSF amyloid-β and tau protein levels, showed patterns of cortical thickness and subcortical volumes not significantly different from healthy controls, but highly different from patients with MCI, either due to AD or not.
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