Evidence map›Paper›PMID 32322821›Full record

ArticleBrain communications2020

Adenosine kinase inhibition promotes proliferation of neural stem cells after traumatic brain injury.

Hoda M Gebril, Rizelle Mae Rose, Raey Gesese, Martine P Emond, Yuqing Huo, Eleonora Aronica, Detlev Boison

Open access · goldAbstract read
In one paragraph

Article in Brain communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Adenosine Kinase: An Epigenetic Modulator and Drug Target.Journal of inherited metabolic disease · 2025
    Review
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  13. Adenosine AJournal of neuroinflammation · 2020
    Article
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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

7 authors at 4 institutions in 2 countries.

Hoda M GebrilDepartment of Neurosurgery, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ 08854, USA.
Rizelle Mae RoseRobert Stone Dow Neurobiology Laboratories, Legacy Research Institute, Portland, OR 97232, USA.
Raey GeseseRobert Stone Dow Neurobiology Laboratories, Legacy Research Institute, Portland, OR 97232, USA.
Martine P EmondRobert Stone Dow Neurobiology Laboratories, Legacy Research Institute, Portland, OR 97232, USA.
Yuqing HuoDepartment of Cellular Biology & Anatomy, Medical College of Georgia, Vascular Biology Center, Augusta University, Augusta, GA 30912, USA.
Eleonora AronicaDepartment of (Neuro)Pathology, Academic Medical Center and Swammerdam Institute for Life Sciences, Center for Neuroscience, University of Amsterdam, Amsterdam, The Netherlands.
Detlev BoisonDepartment of Neurosurgery, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ 08854, USA.ORCID 0000-0001-5797-9406
Legacy Health · USRutgers, The State University of New Jersey · USAugusta University · USNetherlands Institute for Neuroscience · NL

Funding

The Role of Adenosine in Ketogenic Diet TherapyR01NS065957 · NINDS · TRINITY COLLEGE · PI BOISON, DETLEV, GEIGER, JONATHAN DAVID · 2010 to 2021
$3.9M
Adenosine receptor mediated therapies for SUDEPR01NS103740 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI BOISON, DETLEV · 2018 to 2022
$1.7M
NINDS NIH HHS R01 NS065957NINDS NIH HHS R01 NS103740
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a major public health concern and remains a leading cause of disability and socio-economic burden. To date, there is no proven therapy that promotes brain repair following an injury to the brain. In this study, we explored the role of an isoform of adenosine kinase expressed in the cell nucleus (ADK-L) as a potential regulator of neural stem cell proliferation in the brain. The rationale for this hypothesis is based on coordinated expression changes of ADK-L during foetal and postnatal murine and human brain development indicating a role in the regulation of cell proliferation and plasticity in the brain. We first tested whether the genetic disruption of ADK-L would increase neural stem cell proliferation after TBI. Three days after TBI, modelled by a controlled cortical impact, transgenic mice, which lack ADK-L (ADK

Indexed as

adenosine kinasedentate gyrusneurogenesisregenerationTraumatic brain injury

Identifiers

PMID32322821
PMCPMC7158236
OpenAlexW3007891830

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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 OpenQuestion graph.