Evidence map›Paper›PMID 39614299›Full record

ArticleActa neuropathologica communications2024

Spatial transcriptomics in focal cortical dysplasia type IIb.

Yujiao Wang, Yihe Wang, Linai Guo, Chunhao Shen, Yongjuan Fu, Penghu Wei, Yongzhi Shan, Qian Wu, Yue-Shan Piao, Guoguang Zhao

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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

10 authors.

Yujiao Wang *Department of Pathology, Xuanwu Hospital, Capital Medical University, Beijing Municipal Geriatric Medical Research Center, Beijing, 100053, China.
Yihe Wang *Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
Linai Guo *Department of Pathology, Xuanwu Hospital, Capital Medical University, Beijing Municipal Geriatric Medical Research Center, Beijing, 100053, China.
Chunhao ShenDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
Yongjuan FuDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Beijing Municipal Geriatric Medical Research Center, Beijing, 100053, China.
Penghu WeiDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
Yongzhi ShanDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
Qian WuState Key Laboratory of Cognitive Neuroscience and Learning, Beijing Normal University, Beijing, 100875, China.
Yue-Shan PiaoDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Beijing Municipal Geriatric Medical Research Center, Beijing, 100053, China. yueshanpiao@126.com.
Guoguang ZhaoDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. ggzhao@vip.sina.com.

Funding

Foundation of China No. 82030037Fundamental Research Program of Shanxi Province No. 202203021222364the Translational and Application Project of Brain-inspired and Network Neuroscience on Brain Disorders, Beijing Municipal Health Commission No. 11000022T000000444685
6 · The paper itself

Abstract

Focal cortical dysplasia (FCD) type IIb (FCD IIb) is an epileptogenic malformation of the neocortex that is characterized by cortical dyslamination, dysmorphic neurons (DNs) and balloon cells (BCs). Approximately 30-60% of lesions are associated with brain somatic mutations in the mTOR pathway. Herein, we investigated the transcriptional changes around the DNs and BCs regions in freshly frozen brain samples from three patients with FCD IIb by using spatial transcriptomics. We demonstrated that the DNs region in a gene enrichment network enriched for the mTOR signalling pathway, autophagy and the ubiquitin‒proteasome system, additionally which are involved in regulating membrane potential, may contribute to epileptic discharge. Moreover, differential expression analysis further demonstrated stronger expression of components of the inflammatory response and complement activation in the BCs region. And the DNs and BCs regions exhibited common functional modules, including regulation of cell morphogenesis and developmental growth. Furthermore, the expression of representative proteins in the functional enrichment module mentioned above was increased in the lesions of FCD IIb, such as p62 in DNs and BCs, UCHL1 in DNs, and C3 and CLU in BCs, which was confirmed via immunohistochemistry. Collectively, we constructed a spatial map showing the potential effects and functions of the DNs and BCs regions at the transcriptomic level and generated publicly available data on human FCD IIb to facilitate future research on human epileptogenesis.

Indexed as

Malformations of Cortical Development, Group ITranscriptomeChildChild, PreschoolComplement C3EpilepsyFemaleFocal Cortical DysplasiaHumansMaleNeuronsSequestosome-1 ProteinTOR Serine-Threonine KinasesUbiquitin ThiolesteraseComplement C3Sequestosome-1 ProteinSQSTM1 protein, humanTOR Serine-Threonine KinasesUbiquitin ThiolesteraseUCHL1 protein, humanComplement activationDrug-resistant epilepsyFocal cortical dysplasia type IIInflammatory responseRegulation of membrane potentialSpatial transcriptomics

Identifiers

PMID39614299
PMCPMC11607982

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.