In one paragraphArticle in bioRxiv : the preprint server for biology, 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
14 authors.
Alexandra I MotDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0003-3180-6405 Ying LiBrain Science Institute, Departments of Neurology and Neuroscience, Johns Hopkins University, Baltimore MD, USA.ORCID 0009-0005-3885-5201 Payam DibajDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0003-1585-6330 Iva D TzvetanovaDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0009-0002-1206-6202 Ulrike C GerwigDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.
Tizibt A BogaleDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0002-0905-2654 Sandra GoebbelsDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0001-8343-9972 Wiebke MöbiusDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0002-2902-7165 Dwight E BerglesBrain Science Institute, Departments of Neurology and Neuroscience, Johns Hopkins University, Baltimore MD, USA.ORCID 0000-0002-7133-7378 Brett M MorrisonBrain Science Institute, Departments of Neurology and Neuroscience, Johns Hopkins University, Baltimore MD, USA.ORCID 0000-0001-5404-3899 Jeffrey D RothsteinBrain Science Institute, Departments of Neurology and Neuroscience, Johns Hopkins University, Baltimore MD, USA.ORCID 0000-0003-2001-8470 Don W ClevelandDepartment of Molecular and Cellular Medicine, University of California at San Diego, La Jolla, CA 92093 USA.ORCID 0000-0002-1934-3682 Julia M EdgarDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0002-3869-0962 Klaus-Armin NaveDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0001-8724-9666 Funding
Neuronal vs. glial glutamate transport regulation in ALSR01NS033958 · NINDS · JOHNS HOPKINS UNIVERSITY · PI ROTHSTEIN, JEFFREY D · 1995 to 2013
$5.4MOligodendroglial Dysfunction in C9orf72 ALS and FTDR01NS099320 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MORRISON, BRETT M., ROTHSTEIN, JEFFREY D · 2017 to 2021
$3.0MNINDS NIH HHS R01 NS033958NINDS NIH HHS R01 NS099320
6 · The paper itselfAbstract
Amyotrophic lateral sclerosis (ALS) is a highly debilitating and fatal disease characterized by the progressive loss of motor neurons. Reduced oligodendroglial support has been implicated in ALS progression but remains mechanistically unexplained. Here, using a mutant superoxide dismutase 1 (SOD1-G37R) mouse model of familial ALS, Cre-mediated excision of the mutant SOD1 gene within the oligodendrocyte lineage prior to myelin compaction is shown to slow disease onset, improve motor performance, and prolong survival. In contrast, silencing mutant
Indexed as
Amyotrophic lateral sclerosis (ALS)axonal metabolic supportBiological Sciencesmyelinic nanochannelsNeuroscienceoligodendrocytesuperoxide dismutase 1 (SOD1)
Identifiers
PMID42327318
PMCPMC13277883
What OpenQuestion holds
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