: 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.

Late-onset temporal lobe epilepsy: insights from brain atrophy and Alzheimer's disease biomarkers / Ballerini, Alice; Biagioli, Niccolò; Carbone, Chiara; Chiari, Annalisa; Tondelli, Manuela; Vinceti, Giulia; Bedin, Roberta; Malagoli, Marcella; Genovese, Maurilio; Scolastico, Simona; Giovannini, Giada; Pugnaghi, Matteo; Orlandi, Niccolò; Lemieux, Louis; Meletti, Stefano; Zamboni, Giovanna; Vaudano, Anna Elisabetta. - In: BRAIN. - ISSN 1460-2156. - (2024), pp. 0-10. [10.1093/brain/awae207]

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

Ballerini, Alice;Biagioli, Niccolò;Carbone, Chiara;Chiari, Annalisa;Tondelli, Manuela;Vinceti, Giulia;Bedin, Roberta;Malagoli, Marcella;Genovese, Maurilio;Scolastico, Simona;Giovannini, Giada;Pugnaghi, Matteo;Orlandi, Niccolò;Lemieux, Louis;Meletti, Stefano;Zamboni, Giovanna;Vaudano, Anna Elisabetta
2024

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 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.
2024
0
10
Late-onset temporal lobe epilepsy: insights from brain atrophy and Alzheimer's disease biomarkers / Ballerini, Alice; Biagioli, Niccolò; Carbone, Chiara; Chiari, Annalisa; Tondelli, Manuela; Vinceti, Giulia; Bedin, Roberta; Malagoli, Marcella; Genovese, Maurilio; Scolastico, Simona; Giovannini, Giada; Pugnaghi, Matteo; Orlandi, Niccolò; Lemieux, Louis; Meletti, Stefano; Zamboni, Giovanna; Vaudano, Anna Elisabetta. - In: BRAIN. - ISSN 1460-2156. - (2024), pp. 0-10. [10.1093/brain/awae207]
Ballerini, Alice; Biagioli, Niccolò; Carbone, Chiara; Chiari, Annalisa; Tondelli, Manuela; Vinceti, Giulia; Bedin, Roberta; Malagoli, Marcella; Genove...espandi
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1352527
Citazioni
  • ???jsp.display-item.citation.pmc??? 0
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact