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Preparing Undercut Model of Posttraumatic Epileptogenesis in Rodents
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Microglial GPR35 Ameliorates Epileptogenesis and Neuroinflammation via PDGFA Domain 2 Signaling
Qi Wang1,2, Tingting Qu1,3, Qibing Sun1
1Department of Neurology, Epilepsy and Headache Group, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|January 28, 2026
Summary
Microglial GPR35 activation suppresses neuroinflammation and seizures in epilepsy by regulating platelet-derived growth factor A (PDGFA). Targeting GPR35 offers a dual therapy for epilepsy, reducing seizures and cognitive issues.
Area of Science:
- Neuroimmunology
- Epilepsy Pathophysiology
- Molecular Signaling
Background:
- Neuroinflammation drives epilepsy and cognitive decline.
- Current anti-inflammatory treatments for epilepsy are limited.
Purpose of the Study:
- Investigate the role of microglial GPR35 in epilepsy.
- Determine the mechanism of GPR35-mediated neuroinflammation and epileptogenesis.
Main Methods:
- Single-nucleus RNA sequencing in temporal lobe epilepsy (TLE) patients and models.
- Pharmacological modulation of GPR35.
- Assessment of seizure susceptibility and cognitive function.
- Analysis of PDGFA degradation and PI3K-AKT signaling.
Main Results:
- GPR35 is upregulated in disease-associated microglia in TLE.
- GPR35 deficiency worsens seizures and cognitive deficits.
- GPR35 activation reduces seizures, neuroinflammation, and cognitive deficits.
- GPR35 interacts with PDGFA, inhibiting its degradation and activating PI3K-AKT signaling, suppressing inflammation.
Conclusions:
- Microglial GPR35 orchestrates neuroinflammation in epilepsy via PDGFA signaling.
- GPR35 is a druggable target for treating epilepsy and its cognitive comorbidities.
- Targeting GPR35 disrupts the cycle of inflammation and hyperexcitability in epilepsy.
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