Article in Glia, 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.
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
15 authors.
Werner DykstraDepartment of Translational Neuroscience, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, the Netherlands.ORCID 0000-0002-7663-4689
Zuzana MatusovaLaboratory of Glial Biology and Omics Technologies, Institute of Biotechnology of the Czech Academy of Sciences, Vestec, Czech Republic.ORCID 0000-0002-5014-5801
Rachel A BattagliaDepartment of Cell Biology and Physiology, University of North Carolina, Chapel Hill, North Carolina, USA.ORCID 0000-0003-3187-6964
Pavel AbaffyLaboratory of Glial Biology and Omics Technologies, Institute of Biotechnology of the Czech Academy of Sciences, Vestec, Czech Republic.ORCID 0000-0002-7571-8880
Nuria Goya-IglesiasCentro de Investigaciones Biológicas Margarita Salas, C.S.I.C., Madrid, Spain.ORCID 0009-0003-5830-1287
Dolores Pérez-SalaCentro de Investigaciones Biológicas Margarita Salas, C.S.I.C., Madrid, Spain.ORCID 0000-0003-0600-665X
Henrik AhleniusStem Cells, Aging and Neurodegeneration, Lund Stem Cell Center, Department of Experimental Medical Science, Faculty of Medicine, Lund University, Lund, Sweden.ORCID 0000-0001-8958-6148
Mikael KubistaLaboratory of Gene Expression, Institute of Biotechnology of the Czech Academy of Sciences, Vestec, Czech Republic.ORCID 0000-0002-2940-352X
R Jeroen PasterkampDepartment of Translational Neuroscience, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, the Netherlands.ORCID 0000-0003-1631-6440
Li LiDepartment of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, Duarte, California, USA.ORCID 0000-0001-7886-6056
Jianfei ChaoDepartment of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, Duarte, California, USA.ORCID 0000-0003-4607-9925
Yanhong ShiDepartment of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, Duarte, California, USA.ORCID 0000-0002-3938-5839
Lukas ValihrachLaboratory of Glial Biology and Omics Technologies, Institute of Biotechnology of the Czech Academy of Sciences, Vestec, Czech Republic.ORCID 0000-0002-6704-4337
Milos PeknyLaboratory of Astrocyte Biology and CNS Regeneration, Center of Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gotenburg, Sweden.ORCID 0000-0003-1607-8075
Elly M HolDepartment of Translational Neuroscience, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, the Netherlands.ORCID 0000-0001-5604-2603
Funding
Agencia Estatal de Investigación 10.13039/501100011033ALF Gothenburg 146051ALF Gothenburg 965939Amlöv's FoundationComunidad Autónoma de Madrid PIPF-2022/SAL-GL-25771Czech science foundation 24-11364SCzech science foundation 24-12028SEuropean Joint Programme on Rare Diseases EJP RD 2019 ALEXANDERInstitute of Biotechnology of the Czech Academy of Sciences (IBT CAS) institutional support RVO 86652036'la Caixa' Foundation LCF/PR/HR21/52410002MICIN and ERDF PID2021-126827OB-I00MICIN and ERDF RTI2018-097624-B-I00Petrus och Augusta Hedlunds Stiftelse M2018-0803Petrus och Augusta Hedlunds Stiftelse M-2019-1026Söderberg's FoundationsSvenska Sällskapet för Medicinsk Forskning FO02021-0082Svenska Sällskapet för Medicinsk Forskning FO2022-1032Vetenskapsrådet 2018-02695Vetenskapsrådet 2019-00284Vetenskapsrådet 2020-01148ZonMw 463002004
6 · The paper itself
Abstract
Glial fibrillary acidic protein (GFAP) is a type-3 intermediate filament protein mainly expressed in astrocytes in the central nervous system. Mutations in GFAP cause Alexander disease (AxD), a rare and fatal neurological disorder. How exactly mutant GFAP eventually leads to white and gray matter deterioration in AxD remains unknown. GFAP is known to be expressed also in neural precursor cells in the developing brain. Here, we used AxD patient-derived induced pluripotent stem cells (iPSCs) to explore the impact of mutant GFAP during neurodifferentiation. Our results show that GFAP is already expressed in iPSCs. Moreover, we have found that mutations in GFAP can severely affect neural organoid development through altering lineage commitment in embryoid bodies. Together, these results support the notion that GFAP plays a role as an early modulator of neurodevelopment.
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.
Mutations in GFAP Alter Early Lineage Commitment of Organoids. · full record | OpenQuestion