Evidence map›Paper›PMID 40313715›Full record

ArticleFrontiers in cell and developmental biology2025

Critical contributions of neuronal subtypes to pediatric drug-resistant focal dysplasia.

Yujie Zhang, Lin Li, Fengjun Zhu, Xinyang Zhang, Dan Xia, Qiuling Miao, Cheng Zhong, Shuli Liang, Dezhi Cao, Huafang Zou and 7 more

Abstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Yujie Zhang *Pediatric Neurology, Shenzhen Children's Hospital, Shenzhen, China.
Lin Li *Surgery Division, Epilepsy Center, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Fengjun Zhu *Surgery Division, Epilepsy Center, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Xinyang ZhangState Key Laboratory of Chemical Oncogenomics, Shenzhen Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China.
Dan XiaCellular and Molecular Diagnostics Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Qiuling MiaoDepartment of Pathology, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Cheng ZhongState Key Laboratory of Brain Cognition and Brain-inspired Intelligence Technology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, China.
Shuli LiangFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, China.
Dezhi CaoPediatric Neurology, Shenzhen Children's Hospital, Shenzhen, China.
Huafang ZouSurgery Division, Epilepsy Center, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Jing DuanPediatric Neurology, Shenzhen Children's Hospital, Shenzhen, China.
Yousheng ShuState Key Laboratory of Medical Neurobiology, Institute for Translational Brain Research, MOE Frontier Center for Brain Science, Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Yi YaoSurgery Division, Epilepsy Center, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Jianming SongDepartment of Pathology, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Songnian HuState Key Laboratory of Microbial Resources, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Jianxiang LiaoPediatric Neurology, Shenzhen Children's Hospital, Shenzhen, China.
Qiang ZhouState Key Laboratory of Chemical Oncogenomics, Shenzhen Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Approximately 75% of epilepsy cases emerge in childhood, and 10%-30% of these pediatric epilepsy cases are resistant to standard drug therapies; however, the underlying causes of resistance remain poorly understood. Focal cortical dysplasia (FCD) is a primary contributor to pediatric epilepsy and is often associated with drug resistance. We performed single-nucleus RNA sequencing (snRNA-seq) and patch-clamp recording of fresh brain tissue samples that were obtained from pediatric FCD patients during surgery. Our study revealed significant transcriptomic changes across multiple subtypes of excitatory neurons and GABAergic neurons. Among the identified neuronal subtypes, the three inhibitory neuronal subtypes PVALB_RGS5, VIP_CRH, and SST_PENK presented prominent transcriptomic alterations related to epilepsy. The expression of genes enriched in epilepsy-related signaling pathways, especially those associated with excitatory/inhibitory (E/I) balance and energy metabolism, was significantly altered in these neuronal subtypes. Differentially expressed genes (DEGs) in the PVALB_RGS5 subtype were particularly enriched in pathways related to synaptic function. Recordings from fast-spiking (FS)/parvalbumin-containing neurons in brain sections from patients with FCD revealed a reduction in excitatory synaptic inputs, which indicates fewer synaptic inputs onto these neurons and lower activity. In addition, astrocyte subtype 4 exhibited distinct metabolic characteristics and interaction patterns with neuronal subtypes, which suggests their significant role in epilepsy pathophysiology. Our findings indicate that several specific neuronal and astrocyte subtypes play critical roles in the genesis and/or progression of drug-resistant pediatric seizures and that targeting these subtypes may represent a new treatment option.

Indexed as

drug-resistant epilepsyenergy metabolismfast-spiking neuronfocal cortical dysplasianeuronal subtypes

Identifiers

PMID40313715
PMCPMC12043673

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