TY - JOUR
T1 - Alzheimer's disease and late-onset epilepsy of unknown origin
T2 - two faces of beta amyloid pathology
AU - Costa, Cinzia
AU - Romoli, Michele
AU - Liguori, Claudio
AU - Farotti, Lucia
AU - Eusebi, Paolo
AU - Bedetti, Chiara
AU - Siliquini, Sabrina
AU - Cesarini, Elena Nardi
AU - Romigi, Andrea
AU - Mercuri, Nicola B.
AU - Parnetti, Lucilla
AU - Calabresi, Paolo
PY - 2018/9/18
Y1 - 2018/9/18
N2 - 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.
AB - 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.
KW - Alzheimer's disease
KW - Beta amyloid
KW - CSF biomarkers
KW - Dementia
KW - Epilepsy
UR - http://www.scopus.com/inward/record.url?scp=85055031124&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85055031124&partnerID=8YFLogxK
U2 - 10.1016/j.neurobiolaging.2018.09.006
DO - 10.1016/j.neurobiolaging.2018.09.006
M3 - Article
C2 - 30317034
AN - SCOPUS:85055031124
VL - 73
SP - 61
EP - 67
JO - Neurobiology of Aging
JF - Neurobiology of Aging
SN - 0197-4580
ER -