The Role of Neuroinflammation and Network Anomalies in Drug-Resistant Epilepsy.
10.1007/s12264-025-01348-w
- Author:
Jianwei SHI
1
;
Jing XIE
2
;
Zesheng LI
1
;
Xiaosong HE
3
;
Penghu WEI
4
;
Josemir W SANDER
5
;
Guoguang ZHAO
6
Author Information
1. Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
2. Deanery of Biomedical Sciences, Edinburgh Medical School, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, EH8 9AG, UK.
3. Department of Psychology, University of Science and Technology of China, Hefei, 230022, China.
4. Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. weipenghu@xwhosp.org.
5. Department of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK. l.sander@ucl.ac.uk.
6. Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. ggzhao@vip.sina.com.
- Publication Type:Review
- Keywords:
Brain network;
Chronicity;
Epilepsy;
Neuro-immune interaction;
Neuroglia
- MeSH:
Humans;
Drug Resistant Epilepsy/metabolism*;
Neuroinflammatory Diseases/immunology*;
Animals;
Brain/pathology*;
Nerve Net/pathology*
- From:
Neuroscience Bulletin
2025;41(5):881-905
- CountryChina
- Language:English
-
Abstract:
Epilepsy affects over 50 million people worldwide. Drug-resistant epilepsy (DRE) accounts for up to a third of these cases, and neuro-inflammation is thought to play a role in such cases. Despite being a long-debated issue in the field of DRE, the mechanisms underlying neuroinflammation have yet to be fully elucidated. The pro-inflammatory microenvironment within the brain tissue of people with DRE has been probed using single-cell multimodal transcriptomics. Evidence suggests that inflammatory cells and pro-inflammatory cytokines in the nervous system can lead to extensive biochemical changes, such as connexin hemichannel excitability and disruption of neurotransmitter homeostasis. The presence of inflammation may give rise to neuronal network abnormalities that suppress endogenous antiepileptic systems. We focus on the role of neuroinflammation and brain network anomalies in DRE from multiple perspectives to identify critical points for clinical application. We hope to provide an insightful overview to advance the quest for better DRE treatments.
