Emerging Role of Microglia-Mediated Neuroinflammation in Epilepsy after Subarachnoid Hemorrhage
- 26 January 2021
- journal article
- review article
- Published by Springer Science and Business Media LLC in Molecular Neurobiology
- Vol. 58 (6), 2780-2791
- https://doi.org/10.1007/s12035-021-02288-y
Abstract
Epilepsy is a common and serious complication of subarachnoid hemorrhage (SAH), giving rise to increased morbidity and mortality. It's difficult to identify patients at high risk of epilepsy and the application of anti-epileptic drugs (AEDs) following SAH is a controversial topic. Therefore, it's pressingly needed to gain a better understanding of the risk factors, underlying mechanisms and the optimization of therapeutic strategies for epilepsy after SAH. Neuroinflammation, characterized by microglial activation and the release of inflammatory cytokines, has drawn growing attention due to its influence on patients with epilepsy after SAH. In this review, we discuss the risk factors for epilepsy after SAH and emphasize the critical role of microglia. Then we discuss how various molecules arising from pathophysiological changes after SAH activate specific receptors such as TLR4, NLRP3, RAGE, P2X7R and initiate the downstream inflammatory pathways. Additionally, we focus on the significant responses implicated in epilepsy including neuronal excitotoxicity, the disruption of blood-brain barrier (BBB) and the change of immune responses. As the application of AEDs for seizure prophylaxis after SAH remains controversial, the regulation of neuroinflammation targeting the key pathological molecules could be a promising therapeutic method. While neuroinflammation appears to contribute to epilepsy after SAH, more comprehensive experiments on their relationships are needed.Keywords
Funding Information
- Natural Science Fund of Guangdong Province (2017A030313597)
- “Climbing Program” Special Fund of Guangdong Province (pdjh2019b0100, pdjh2020b0112)
- Southern Medical University (LX2016N006, KJ20161102, 201912121004S, 201912121013, S202012121088, X202012121354,19NJ-YB03)
This publication has 113 references indexed in Scilit:
- Toll-like receptor 4 signaling in intracerebral hemorrhage-induced inflammation and injuryJournal of Neuroinflammation, 2013
- Albumin is taken up by hippocampal NG2 cells and astrocytes and decreases gap junction couplingEpilepsia, 2012
- High-mobility group box-1 impairs memory in mice through both toll-like receptor 4 and Receptor for Advanced Glycation End ProductsExperimental Neurology, 2011
- Endotoxin-activated microglia injure brain derived endothelial cells via NF-κB, JAK-STAT and JNK stress kinase pathwaysJournal of Inflammation, 2011
- A Two-Way Communication between Microglial Cells and Angiogenic Sprouts Regulates Angiogenesis in Aortic Ring CulturesPLOS ONE, 2011
- Upregulation of inward rectifier K+(Kir2) channels in dentate gyrus granule cells in temporal lobe epilepsyJournal Of Physiology-London, 2009
- Astrocytic Dysfunction in Epileptogenesis: Consequence of Altered Potassium and Glutamate Homeostasis?Journal of Neuroscience, 2009
- Tumor necrosis factor‐α‐induced neutral sphingomyelinase‐2 modulates synaptic plasticity by controlling the membrane insertion of NMDA receptorsJournal of Neurochemistry, 2009
- Seizures and Epilepsy following Aneurysmal Subarachnoid Hemorrhage : Incidence and Risk FactorsJournal of Korean Neurosurgical Society, 2009
- A novel non-transcriptional pathway mediates the proconvulsive effects of interleukin-1Brain, 2008