Evidence map›Paper›PMID 42834251›Full record

ArticleMolecular neurobiology2026

Low Dose NeuroD1 Delivery in Mouse TBI Models.

Isaac H Clark, Ansharah Khan, Christopher With, Zachary Roushdy, Dilmareth Natera-Rodriguez, Kevin Sun, Olivia Erlanson, Shaimaa Khedr, Walter C Low, Andrew W Grande

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In one paragraph

Article in Molecular neurobiology, 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

10 authors.

Isaac H ClarkBiomedical Engineering Graduate Program, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA. clark.isaac@mayo.edu.
Ansharah KhanDepartment of Neurosurgery, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA.
Christopher WithDepartment of Neurosurgery, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA.
Zachary RoushdyDepartment of Neurosurgery, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA.
Dilmareth Natera-RodriguezDepartment of Neurosurgery, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA.
Kevin SunGraduate Program in Neuroscience, University of Minnesota, Minneapolis, MN, 55455, USA.
Olivia ErlansonDepartment of Neurosurgery, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA.
Shaimaa KhedrDepartment of Neurosurgery, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA.
Walter C LowBiomedical Engineering Graduate Program, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA.
Andrew W GrandeBiomedical Engineering Graduate Program, University of Minnesota, 2001 Sixth St., SE, Minneapolis, MN, 55455, USA. grande@umn.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) often results in serious neuronal tissue damage that can lead to progressive neurological impairment. NeuroD1, a transcription factor involved in neuronal differentiation, may be able to facilitate recovery post-TBI through the promotion of both neuroprotection and astrocyte-to-neuron reprogramming. The efficacy and optimal parameters for NeuroD1-based treatment, however, remain uncertain. This study investigated the effects of AAV-mediated NeuroD1 delivery in TBI mouse models, focusing on cellular reprogramming at low dosages. Dose response experiments revealed that lower viral doses provided the greatest transduction specificity. Notably, lower viral titers resulted in greater astrocyte-specific transduction whereas higher titers increased transduction in off-targets (neurons), potentially due to toxicity and/or leakage. Using these low dosages, our findings indicate that NeuroD1 treatment did not produce statistically significant structural restoration, nor did it greatly alter neuroinflammation measures; however, it did allow for functional improvement in beam walk performance, suggesting enhanced neurological recovery. Prospective studies should refine experimental conditions, incorporate a broader range of behavioral assessments, and explore combination therapies to enhance both functional and structural recovery. NeuroD1-based interventions remain a promising avenue for promoting functional improvement following TBI, although further research is required to drive these findings to clinical applications.

Indexed as

Basic Helix-Loop-Helix ProteinsBrain Injuries, TraumaticGene Transfer TechniquesAnimalsAstrocytesDependovirusDisease Models, AnimalMaleMiceMice, Inbred C57BLNeuronsRecovery of FunctionTransduction, GeneticBasic Helix-Loop-Helix ProteinsNeurod1 protein, mouseNeuroD1Neuronal differentiationTraumatic brain injury

Identifiers

PMID42834251
PMCPMC13638745

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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.