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Epilepsy and Seizures: Overview

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Epilepsy is a chronic neurological disease marked by recurrent, unpredictable seizures. These seizures are caused by abnormal electrical discharges in the brain, leading to behavior, sensation, or consciousness alterations. They can also cause transient impairment of awareness, interfering with daily activities.
Various factors can trigger epilepsy, including genetic factors, brain damage, metabolic causes, and unknown etiology. Diagnosis of epilepsy involves electroencephalography (EEG), which...

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A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

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Elevated Apolipoprotein E Expression in Hippocampal Microglia Drives Temporal Lobe Epilepsy Progression.

Jianwei Shi^1,2,3, Zesheng Li^1,2,3, Xin Sun⁴

¹Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, No. 45 Changchun Road, Beijing, 100053, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|October 14, 2025

Summary

Apolipoprotein E (APOE) drives temporal lobe epilepsy (TLE) progression by activating microglia in the hippocampus. Targeting APOE and its pathways offers a promising therapeutic strategy for TLE and hippocampal sclerosis.

Keywords:

apolipoprotein E metabolomics microglia neuroinflammation neuronal excitability temporal lobe epilepsy

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Lipidomics and Transcriptomics in Neurological Diseases

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Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

Area of Science:

Neuroscience
Immunology
Metabolomics

Background:

Temporal lobe epilepsy (TLE) is the most common epilepsy type, often involving hippocampal sclerosis (HS).
Microglia reactivity is key in TLE pathogenesis, with apolipoprotein E (APOE) potentially mediating these effects.
The precise role of APOE in TLE progression and hippocampal microglia remains unclear.

Purpose of the Study:

To elucidate the role of APOE and hippocampal microglia in TLE mechanisms.
To validate APOE as a potential biomarker and therapeutic target for TLE.

Main Methods:

Bioinformatics analysis of patient and mouse model data.
Single-cell RNA sequencing to identify APOE-expressing microglia.
In vitro and in vivo functional experiments in TLE mouse models.
Genetic knockout of APOE in TLE models.

Main Results:

APOE expression is significantly elevated in TLE-HS hippocampi and mouse models.
A subset of microglia highly expresses APOE, increasing during disease progression.
APOE-expressing microglia promote neuroinflammation, neuronal apoptosis, and excitability, altering glycerophospholipid metabolism.
APOE knockout reduces gliosis, neuronal death, and seizures in TLE mice.

Conclusions:

APOE-expressing microglia are critical drivers of hippocampal sclerosis and TLE progression.
APOE and its downstream pathways represent promising therapeutic targets for TLE.