Evidence map›Paper›PMID 40947439›Full record

ArticleNeuroscience bulletin2026

Dysregulation of the BRD2-FGF17 Signal Pathway Induces Abnormal Forebrain Development Associated with Schizophrenia.

Xiao Yu, Jiacheng Du, Chenger Zhou, Yongheng Huang, Huijuan Li, Bruce M Cohen, Sangmi Chung, Zhicheng Shao

Abstract read
PubMed Full text at PMC Publisher
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. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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.

Xiao YuDepartment of Neurology, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Zhongshan Hospital, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China.ORCID http://orcid.org/0009-0009-3230-8580
Jiacheng DuDepartment of Neurology, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Zhongshan Hospital, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China.
Chenger ZhouDepartment of Neurology, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Zhongshan Hospital, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China.
Yongheng HuangDepartment of Neurology, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Zhongshan Hospital, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China.
Huijuan LiDepartment of Neurology, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Zhongshan Hospital, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China.
Bruce M CohenDepartment of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, 02478, USA.
Sangmi ChungDepartment of Cell Biology and Anatomy, New York Medical College, Valhalla, NY, 10595, USA.
Zhicheng ShaoDepartment of Neurology, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Zhongshan Hospital, Institute for Translational Brain Research, Fudan University, Shanghai, 200032, China. zcshao@fudan.edu.cn.ORCID http://orcid.org/0000-0003-4383-119X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia (SCZ) is a severe and hereditary neurodevelopmental disorder with unknown etiology. Here, we found that the SCZ risk gene BRD2, as an epigenetic reader, is consistently expressed in developing mouse and human cortical astrocytes. Astrocyte-specific Brd2 knockout in mice leads to dysregulation of immune responses and reduces Fgf17 expression, resulting in SCZ-like behaviors, including impaired sensorimotor gating, memory, and cognitive deficits. Moreover, BRD2 inhibition using JQ1 in forebrain organoids leads to FGF17 reduction, inducing developmental deficits involved in neural patterning and gliogenesis. The decrease of FGF17 expression was also found in SCZ patient-derived forebrain organoids, similar to BRD2-inhibited forebrain organoids. FGF17 treatment partially rescued the disrupted gene expression in BRD2-inhibited human forebrain organoids. Taken together, these findings suggest that disrupting the BRD2-FGF17 signaling pathway in early brain development may contribute to the pathogenesis of schizophrenia and may represent a potential therapeutic target for SCZ.

Indexed as

Fibroblast Growth FactorsProsencephalonProtein Serine-Threonine KinasesSchizophreniaSignal TransductionAnimalsAstrocytesBromodomain Containing ProteinsHumansMaleMiceMice, Inbred C57BLMice, KnockoutOrganoidsTranscription FactorsBRD2 protein, humanBrd2 protein, mouseBromodomain Containing ProteinsFibroblast Growth FactorsProtein Serine-Threonine KinasesTranscription FactorsBrain organoidBRD2FGF17Forebrain developmentSchizophrenia

Identifiers

PMID40947439
PMCPMC13031458

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.