ArticleNeuropathology and applied neurobiology2025
Increased Incidence of Epilepsy in a Brain Bank Alzheimer's Disease Cohort and Its Association With TDP-43 Pathology.
Article in Neuropathology and applied neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Cognitive and Biomarker Signatures of Late-Onset Temporal Lobe Epilepsy: Toward Non-Alzheimer Neurodegenerative Mechanisms.Neurology · 2026Article
- Tau pathology in epilepsy: emerging mechanisms and translational opportunities.Brain : a journal of neurology · 2026Review
- Epilepsy and EEG abnormalities in neurodegenerative dementias: toward a system epilepsy framework.Frontiers in aging neuroscience · 2026Review
- Increased Incidence of Epilepsy in a Brain Bank Alzheimer's Disease Cohort and Its Association With TDP-43 Pathology.Neuropathology and applied neurobiology · 2025Article
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8 authors.
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Abstract
aimsEvidence suggests Alzheimer's disease (AD) patients are at increased risk of epilepsy and that seizure incidence is associated with faster cognitive decline. Previous studies indicate hyperphosphorylated tau may play a role in this disease association; however, abnormal TDP-43 and α-synuclein deposition have not been extensively examined.
methodsClinical and neuropathological records of AD cases over a 5-year period were retrieved from the London Neurodegenerative Diseases Brain Bank. The 114 cases were categorised into three groups: AD plus epilepsy, AD plus hippocampal sclerosis (HS) and AD only. Semi-quantitative scores for tau, TDP-43 and α-synuclein pathology within the middle temporal gyrus, hippocampus and amygdala were compared between groups.
resultsA 12% incidence of epilepsy and/or epileptic symptomology was found among the cohort. Twelve cases (11%) showed HS. No significant difference in tau pathology scores was seen between groups. However, a significantly higher score for TDP-43 was seen in AD plus epilepsy compared with AD only in the middle temporal gyrus (p = 0.004). The burden of α-synuclein pathology was increased in the amygdala of AD plus epilepsy and AD plus HS.
conclusionsThe incidence of epilepsy within this AD cohort is higher than expected within the general population (even when matched for age), and this may be associated with increased TDP-43 burden. Understanding the relationship between AD and epilepsy may highlight mechanisms of cellular damage and tissue vulnerability.
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