Emerging data suggest a link between Alzheimer’s disease (AD) and epilepsy. AD and other dementias pose increased risk for seizures, with seizure incidence in AD up to ten times greater than in age-matched controls. Mouse models of AD also demonstrate seizures and abnormal spikes or sharp wave discharges (“interictal epileptiform discharges” [IEDs]) on electroencephalography (EEG). Seizures and IEDs may underlie fluctuating cognitive abilities in AD, with the impact of antiseizure medication (ASM) requiring further investigation.
Many epilepsy patients have memory and other cognitive deficits, due to multiple factors. Most adult-onset epilepsy occurs in people =60 years of age, and epilepsy patients are at increased risk of developing dementia. Hyperphosphorylated tau and amyloid deposits were found in resected temporal lobe tissue of epilepsy patients, similar to AD, and increased total and phosphorylated tau levels in the cerebrospinal fluid may predict the onset of AD and other dementias.
The mechanisms underlying the associations between AD, epilepsy, tau deposition, and beta amyloid plaques, and their relationships to clinical features, are unknown. Some epilepsy patients develop dementia, and some AD patients develop seizures, while others do not. Analyses of resected tissue in epilepsy patients also suggest variable amyloid and tau deposition across patients and studies. Who is at risk? What does shared pathology indicate regarding disease development, progression, and treatment? Better understanding of the associations between epilepsy and dementia with respect to epidemiology, pathophysiology, genetics, clinical presentations, and treatment approaches based on animal models and human studies is needed to optimize patient care.
Insight into the relationship between epilepsy and AD requires various approaches, including tissue analysis, imaging, genetic techniques, cognitive testing, and electroencephalography in animals and humans. We welcome manuscripts that span these approaches, including original research articles, brief research articles, clinical trials, case reports, reviews, systematic reviews, mini-reviews, methods articles, hypothesis and theory articles, perspectives, and opinions. Themes may include:
• Diagnosis (e.g., seizure or interictal discharge detection in dementia patients, distinguishing comorbid dementia from epilepsy-related cognitive dysfunction)
• Epidemiology (e.g., incidence and prevalence of comorbid AD and epilepsy, occurrence of epilepsy in other dementias, seizure types, age or stage of onset)
• Genetic risk factors
• Pathophysiology underlying seizure generation in AD and cognitive decline in epilepsy
• Treatment approaches (e.g., effects of ASMs on cognitive decline, impact of disease modifying AD treatments on seizures, neurostimulation)
• What can be learned from other disorders in which cognitive deficits and seizures are common (i.e., traumatic brain injury)
Emerging data suggest a link between Alzheimer’s disease (AD) and epilepsy. AD and other dementias pose increased risk for seizures, with seizure incidence in AD up to ten times greater than in age-matched controls. Mouse models of AD also demonstrate seizures and abnormal spikes or sharp wave discharges (“interictal epileptiform discharges” [IEDs]) on electroencephalography (EEG). Seizures and IEDs may underlie fluctuating cognitive abilities in AD, with the impact of antiseizure medication (ASM) requiring further investigation.
Many epilepsy patients have memory and other cognitive deficits, due to multiple factors. Most adult-onset epilepsy occurs in people =60 years of age, and epilepsy patients are at increased risk of developing dementia. Hyperphosphorylated tau and amyloid deposits were found in resected temporal lobe tissue of epilepsy patients, similar to AD, and increased total and phosphorylated tau levels in the cerebrospinal fluid may predict the onset of AD and other dementias.
The mechanisms underlying the associations between AD, epilepsy, tau deposition, and beta amyloid plaques, and their relationships to clinical features, are unknown. Some epilepsy patients develop dementia, and some AD patients develop seizures, while others do not. Analyses of resected tissue in epilepsy patients also suggest variable amyloid and tau deposition across patients and studies. Who is at risk? What does shared pathology indicate regarding disease development, progression, and treatment? Better understanding of the associations between epilepsy and dementia with respect to epidemiology, pathophysiology, genetics, clinical presentations, and treatment approaches based on animal models and human studies is needed to optimize patient care.
Insight into the relationship between epilepsy and AD requires various approaches, including tissue analysis, imaging, genetic techniques, cognitive testing, and electroencephalography in animals and humans. We welcome manuscripts that span these approaches, including original research articles, brief research articles, clinical trials, case reports, reviews, systematic reviews, mini-reviews, methods articles, hypothesis and theory articles, perspectives, and opinions. Themes may include:
• Diagnosis (e.g., seizure or interictal discharge detection in dementia patients, distinguishing comorbid dementia from epilepsy-related cognitive dysfunction)
• Epidemiology (e.g., incidence and prevalence of comorbid AD and epilepsy, occurrence of epilepsy in other dementias, seizure types, age or stage of onset)
• Genetic risk factors
• Pathophysiology underlying seizure generation in AD and cognitive decline in epilepsy
• Treatment approaches (e.g., effects of ASMs on cognitive decline, impact of disease modifying AD treatments on seizures, neurostimulation)
• What can be learned from other disorders in which cognitive deficits and seizures are common (i.e., traumatic brain injury)
