<scp>KCC2</scp> Dysfunction Mediated by Microglial <scp>BDNF</scp> / <scp>TrkB</scp> Signaling Exacerbates Early Post‐Stroke Seizure Susceptibility

Our findings identify microglia-derived BDNF/TrkB signaling as a critical upstream pathway mediating KCC2 dysfunction in early post-stroke seizure. Targeting this axis by inhibiting microglial activation, blocking TrkB, or directly enhancing KCC2 function with activators like CLP290 represents a promising therapeutic strategy for stroke-related epilepsy.

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Publication Details

Journal
CNS Neuroscience & Therapeutics
Published
2026-02-01
DOI
https://doi.org/10.1002/cns.70795
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
Type
article
Field-Weighted Citation Impact
0.00
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article

KCC2 Dysfunction Mediated by Microglial BDNF / TrkB Signaling Exacerbates Early Post‐Stroke Seizure Susceptibility

Jiangning Yu, Jie Zhou, Kehua Chen, Zhigang Yang et al.
CNS Neuroscience & Therapeutics
Neuroinflammation and Neurodegeneration Mechanisms
article

KCC2 Dysfunction Mediated by Microglial BDNF / TrkB Signaling Exacerbates Early Post‐Stroke Seizure Susceptibility

Jiangning Yu, Jie Zhou, Kehua Chen, Zhigang Yang, Jingyi Cai, Yulong Wang, Mohan Yu, Li Wan, Guoxiang Wang, Yun Wang, Xu Liu, Benjamin H. Wang
article en

Abstract

Our findings identify microglia-derived BDNF/TrkB signaling as a critical upstream pathway mediating KCC2 dysfunction in early post-stroke seizure. Targeting this axis by inhibiting microglial activation, blocking TrkB, or directly enhancing KCC2 function with activators like CLP290 represents a promising therapeutic strategy for stroke-related epilepsy.

CNS Neuroscience & TherapeuticsVol. 32(2)
Fudan University (CN), Integrated Chinese Medicine (China) (HK), Hangzhou Hospital of Traditional Chinese Medicine (CN), Shenzhen Second People's Hospital (CN)
Openalex Percentile: Top 63%
Neuroinflammation and Neurodegeneration Mechanisms
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