ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2023
The multifactorial etiology of cognitive deficits in epilepsy and the neuropathology of mesial temporal lobe epilepsy beyond hyperphosphorylated tau.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Tau pathology in epilepsy: emerging mechanisms and translational opportunities.Brain : a journal of neurology · 2026Review
- Calbindin-D28k deficiency mediates tau-driven hippocampal hyperexcitement and cognitive impairment.Translational neurodegeneration · 2026Article
- The prevalence of chronic traumatic encephalopathy in a historical epilepsy post-mortem collection.Brain pathology (Zurich, Switzerland) · 2025Article
- Hyperphosphorylated Tau and Cognition in Epilepsy.Journal of clinical medicine · 2025Review
- Influence of comorbid anxiety and depression disorder on cognition in older adults with epilepsy.Frontiers in psychiatry · 2025Article
- Neuropathology and epilepsy surgery - 2024 update.Free neuropathology · 2024Article
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3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In response to the recent review by Zawar and Kapur on the overlap between mesial temporal lobe epilepsy (MTLE) and Alzheimer's disease (AD), we (1) underscore that the bidirectionality between epilepsy and dementia is of high interest, also from the epileptological perspective; (2) outline the multifactorial etiology of cognitive deficits in epilepsy; (3) emphasize that the most prevalent neuropathological findings in MTLE comprise hippocampal sclerosis, dysplastic lesions, and neurodevelopmental neoplasm; and (4) state that anti-seizure medication can also have adverse effects on cognition. We conclude that the neuropsychology and neuropathology of MTLE is actually more complex than implicated in the review by Zawar and Kapur. Their suggested model may be valid for a small specific subgroup of cases. However, more studies are needed to confirm the role of hyperphosphorylated tau in epilepsy patients with and without AD considering age and age at epilepsy onset as potential moderator variables.
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