Abstract Details

Title Prevalence and Implications of Neurodegenerative Protein Pathology in Epilepsy and Epileptiform Syndromes: A Systematic Review

Topic Epilepsy/Clinical Neurophysiology (EEG)

Presentation(s) P8 - Poster Session 8 (11:45 AM-12:45 PM)

Poster/Presentation
Number 11-009

Objective Investigation of prevalence and impact of neurodegenerative protein accumulation in epilepsy.

Background Emerging evidence indicates abnormal accumulation of neurodegenerative proteins such as tau and amyloid-β in epilepsy, though their role in cognitive impairment independent of Alzheimer’s disease is uncertain.

Design/Methods Review included peer-reviewed articles from PUBMED MEDLINE, Ovid Medline, Ovid Embase, and Cochrane Central Register of Controlled Trials published before July 7, 2024. Eligible studies included neurodegenerative protein pathology in epilepsy. Only English-language articles were included. This review adhered to PRISMA guidelines, and the risk of bias was assessed using the ROBANS 2 tool.

Results Of 2,071 articles screened, 42 met inclusion criteria, with the majority being retrospective cohorts(n=26). Most studies involved temporal or mesial temporal lobe epilepsy(TLE/MTLE) or drug-resistant epilepsy(DRE) with hippocampal sclerosis. Across studies, 57% of 1,544 patients were male, with mean onset ages ranging from 4.3–25.1 years, mean age at analysis 9–56.5 years, and disease durations of 9.2–42.3 years. Focal impaired awareness seizures predominated, often with secondary generalization. Fourteen studies included DRE populations, with carbamazepine and phenytoin most used. Phosphorylated tau was detected in 3–95% of epilepsy cases across 33 studies, typically elevated in MTLE/HS and associated with older age, longer duration, and poorer cognition. Amyloid pathology appeared in 14 of 25 studies. Cognitive impairment coexisted with neurodegenerative protein accumulation but showed inconsistent correlations.

Conclusions Neurodegenerative protein accumulation, including tau, amyloid-β, is common in epilepsy, especially with chronic or drug-resistant disease. Tau and amyloid were associated with older age, longer epilepsy duration, and cognitive impairment, though correlations with cognition were inconsistent. Epilepsy chronicity, rather than seizure type, appears most strongly linked to protein pathology.

Authors/Disclosures
Syeda Amrah Hashmi, MBBS PRESENTER	Dr. Hashmi has nothing to disclose.
Aleksander Luniewski, MD	Dr. Luniewski has nothing to disclose.
Vanessa Smith (Duke University Health System)	No disclosure on file
Ifrah Zawar, MD (University of virginia)	The institution of Dr. Zawar has received research support from Alzheimer's association. The institution of Dr. Zawar has received research support from American epilepsy society . The institution of Dr. Zawar has received research support from NIH. The institution of Dr. Zawar has received research support from University of Virginia.

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