The multifactorial etiology of cognitive deficits in epilepsy and the neuropathology of mesial temporal lobe epilepsy beyond hyperphosphorylated tau

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.

Automated summary

In response to the review by Zawar and Kapur, we highlight the bidirectionality between epilepsy and dementia, summarize the multifactorial etiology of cognitive deficits in epilepsy, emphasize the prevalent neuropathological findings in MTLE, and state the potential adverse effects of anti-seizure medication on cognition. We conclude that the neuropsychology and neuropathology of MTLE is more complex than suggested in the review, and further studies are needed to explore the role of hyperphosphorylated tau in epilepsy patients with and without AD.