Although amyloid pathology plays a role in epilepsy, little is known about the relationship between beta amyloid and progression to Alzheimer's disease (AD) among patients with late-onset epilepsy of unknown origin (LOEU). This multicenter, observational, prospective study enrolled 40 consecutive nondemented adults diagnosed with LOEU, together with 43 age- and sex-matched healthy controls. All patients completed neuropsychological tests, core CSF AD biomarkers assessment (Aβ1-42, total tau, and phosphorylated tau), and follow-up for a mean of 3 years to verify cognitive decline. Despite age and baseline cognitive performance were similar to healthy controls, patients with LOEU had significant prevalence of CSF pathological Aβ1-42 (<500 pg/mL; 37.5%), 7.5% displaying an AD-like CSF pattern. Moreover, 17.5% of patients with LOEU converted to AD dementia, versus none among healthy controls (p < 0.005). Patients with LOEU with pathological Aβ1-42 had a hazard ratio 3.4 (CI 0.665–17.73) for progression to AD dementia at follow-up. Patients with LOEU have a high prevalence of abnormal CSF Aβ1-42 and progression to AD dementia compared with healthy controls, and therefore should be monitored for cognitive decline.
Costa, C., Romoli, M., Liguori, C., Farotti, L., Eusebi, P., Bedetti, C., Siliquini, S., Cesarini, E. N., Romigi, A., Mercuri, N. B., Parnetti, L., Calabresi, P., Alzheimer's disease and late-onset epilepsy of unknown origin: two faces of beta amyloid pathology, <<NEUROBIOLOGY OF AGING>>, 2019; 73 (January): 61-67. [doi:10.1016/j.neurobiolaging.2018.09.006] [http://hdl.handle.net/10807/171791]
Alzheimer's disease and late-onset epilepsy of unknown origin: two faces of beta amyloid pathology
Calabresi, Paolo
2019
Abstract
Although amyloid pathology plays a role in epilepsy, little is known about the relationship between beta amyloid and progression to Alzheimer's disease (AD) among patients with late-onset epilepsy of unknown origin (LOEU). This multicenter, observational, prospective study enrolled 40 consecutive nondemented adults diagnosed with LOEU, together with 43 age- and sex-matched healthy controls. All patients completed neuropsychological tests, core CSF AD biomarkers assessment (Aβ1-42, total tau, and phosphorylated tau), and follow-up for a mean of 3 years to verify cognitive decline. Despite age and baseline cognitive performance were similar to healthy controls, patients with LOEU had significant prevalence of CSF pathological Aβ1-42 (<500 pg/mL; 37.5%), 7.5% displaying an AD-like CSF pattern. Moreover, 17.5% of patients with LOEU converted to AD dementia, versus none among healthy controls (p < 0.005). Patients with LOEU with pathological Aβ1-42 had a hazard ratio 3.4 (CI 0.665–17.73) for progression to AD dementia at follow-up. Patients with LOEU have a high prevalence of abnormal CSF Aβ1-42 and progression to AD dementia compared with healthy controls, and therefore should be monitored for cognitive decline.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.