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 cerebrospinal fluid (CSF) biomarkers of AD (total and phosphorylated tau, and β-amyloid) 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, twenty 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 a late-onset form of temporal lobe epilepsy, characterized by short disease duration and normal CSF β-amyloid 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 Alzheimer’s Disease or not.

中文翻译：

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迟发性颞叶癫痫：脑萎缩和阿尔茨海默病生物标志物的见解


考虑到世界人口老龄化，老年人癫痫发病率预计将显着增加。有人认为，迟发性颞叶癫痫 (LO-TLE) 的起源可能是神经退行性疾病，并且与阿尔茨海默病 (AD) 重叠。在此，我们的目的是在选定的来源不明的 LO-TLE 人群中表征 AD 的皮质萎缩和脑脊液 (CSF) 生物标志物（总 tau 蛋白、磷酸化 tau 蛋白和 β-淀粉样蛋白）的模式。我们前瞻性地招募了 50 岁后患有颞叶癫痫且无认知障碍的个体。他们接受了结构 MRI 扫描和脑脊液生物标志物测量。将影像学和生物标志物数据与三个回顾性收集的组进行比较：(i) 年龄性别匹配的健康对照，(ii) 患有轻度认知障碍 (MCI) 和脑脊液 AD 生物标志物异常 (MCI-AD) 的患者，以及 (iii) 患者具有 MCI 和正常 CSF AD 生物标志物 (MCI-noAD)。从 52 名患者中，连续招募了 20 名平均病程为 1.8 年的合格 LO-TLE 患者。作为对照人群，纳入了 25 名 MCI-AD 患者、25 名 MCI-noAD 患者和 25 名健康对照。 LO-TLE 中脑脊液生物标志物恢复正常值，与 AD 导致的 MCI 患者显着不同。癫痫患者和健康对照者之间的皮质-皮质下萎缩没有差异，而 MCI 患者则表现出广泛的皮质-皮质下结构损伤。 晚发性颞叶癫痫患者的特点是病程短、脑脊液 β-淀粉样蛋白和 tau 蛋白水平正常，其皮质厚度和皮质下体积模式与健康对照者没有显着差异，但与 MCI 患者有很大不同，无论是否由于阿尔茨海默病。