Evidence map›Paper›PMID 42799825›Full record

ArticleNeuroscience bulletin2026

Disruption of FOXG1 Impairs the Development of Striatal dSPNs, Thereby Contributing to ASD-Like Phenotypes.

Daxiang Xu, Baoshen Zhang, Pengfei Jiang, Pei Zhu, Da Mi, Wei Huang, Ru Ba, Chunjie Zhao

Abstract read
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In one paragraph

Article in Neuroscience bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Daxiang XuKey Laboratory of Developmental Genes and Human Diseases, Ministry of Education, School of Medicine, Southeast University, Nanjing, 210009, China.
Baoshen ZhangKey Laboratory of Developmental Genes and Human Diseases, Ministry of Education, School of Medicine, Southeast University, Nanjing, 210009, China.
Pengfei JiangKey Laboratory of Developmental Genes and Human Diseases, Ministry of Education, School of Medicine, Southeast University, Nanjing, 210009, China.
Pei ZhuKey Laboratory of Developmental Genes and Human Diseases, Ministry of Education, School of Medicine, Southeast University, Nanjing, 210009, China.
Da MiState Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Wei HuangState Key Laboratory of Neuroscience, Institute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China.
Ru BaKey Laboratory of Developmental Genes and Human Diseases, Ministry of Education, School of Medicine, Southeast University, Nanjing, 210009, China. 1093802727@qq.com.ORCID http://orcid.org/0000-0001-6601-2328
Chunjie ZhaoKey Laboratory of Developmental Genes and Human Diseases, Ministry of Education, School of Medicine, Southeast University, Nanjing, 210009, China. zhaocj@seu.edu.cn.ORCID http://orcid.org/0000-0002-7694-6092

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Striatal dysfunction is a feature of autism spectrum disorder (ASD); however, the molecular mechanisms underlying its development remain unclear. Mutations in the transcription factor FOXG1 lead to FOXG1 syndrome, which shares core clinical features with ASD. In the present study, we conditionally deleted Foxg1 in the striatal direct pathway spiny projection neurons (dSPNs) to create Foxg1 conditional knockout (cKO) mice, which we found recapitulated classic ASD-like symptoms, including social deficits, communication impairments, and restricted repetitive behaviors. Loss of FOXG1 further resulted in simplified dendritic arborization and reduced dendritic spine density. We found that FOXG1 drives a set of ASD risk genes, including synaptic receptors and scaffolding proteins, to coordinate the development and function of dSPNs. Further, FOXG1 directly regulated the transcription of GABA

Indexed as

Autism spectrum disorder (ASD)Dendritic developmentDirect pathway spiny projection neurons (dSPNs)Excitation/inhibition balanceForkhead box G1 (FOXG1)GABAB receptorStriatumSynaptic transmission

Identifiers

PMID42799825

What OpenQuestion holds

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Registered trials

None linked

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.