Evidence map›Paper›PMID 30706038›Full record

ArticlePain reports2018

Gene therapy for neuropathic pain using dorsal root ganglion-targeted helper-dependent adenoviral vectors with GAD67 expression.

Nobuhiro Ogawa, Tomoya Terashima, Kazuhiro Oka, Lawrence Chan, Hideto Kojima

Open access · goldAbstract read
In one paragraph

Article in Pain reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Pro-inflammatory microglia-targeted peptide therapy ameliorates neonatal hypoxic-ischemic encephalopathy in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  5. AAV gene therapy vectors in the TMJ.Clinical and experimental dental research · 2022
    Article
  6. Article
  7. Article
  8. High-Capacity Adenoviral Vectors: Expanding the Scope of Gene Therapy.International journal of molecular sciences · 2020
    Review
  9. Review
  10. KLHL1 Controls CaFrontiers in molecular neuroscience · 2019
    Article
  11. 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

5 authors at 2 institutions in 2 countries.

Nobuhiro OgawaDivision of Neurology, Department of Medicine, Shiga University of Medical Science, Otsu, Shiga, Japan.
Tomoya TerashimaDepartment of Stem Cell Biology and Regenerative Medicine, Shiga University of Medical Science, Otsu, Shiga, Japan.
Kazuhiro OkaDepartment of Molecular & Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Lawrence ChanDepartment of Molecular & Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Hideto KojimaDepartment of Stem Cell Biology and Regenerative Medicine, Shiga University of Medical Science, Otsu, Shiga, Japan.
Shiga University of Medical Science · JPBaylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCurrently available medications for neuropathic pain are of limited efficacy. Moreover, they are administered systemically and are associated with significant side effects. Ideally, one can circumvent systemic side effects if such treatment can be administered by delivery of the therapeutic agent directly to the diseased neurons. Towards this end, we previously reported the production of a recombinant helper-dependent adenovirus (HDAd) armed with a tissue-specific homing peptide to deliver transgenes targeting sensory neurons with high efficacy.

objectivesTo develop an effective gene therapy for neuropathic pain by producing a dorsal root ganglion (DRG)-targeted HDAd vector that specifically expresses glutamic acid decarboxylase (GAD) 67 (HDAd-DRG-GAD67).

methodsWe produced spinal nerve transection (SNT) mice as a neuropathic pain model and delivered HDAd-DRG-GAD67 by injection into spinal nerve or intrathecally to these animals. We evaluated the therapeutic efficacy by measuring ion channel gene expression and quantifying mechanical allodynia, a representative symptom of neuropathic pain, in treated animals.

resultsGlutamic acid decarboxylase expression by HDAd-DRG-GAD67 reduced allodynia significantly in SNT mice. In addition, HDAd-DRG-GAD67 had a much greater transduction efficacy and expressed the therapeutic gene for a much longer time and at a lower dose of viral particles than wild-type HDAd. We found that SNT induced the upregulation of Cav3.2 mRNA in the DRG and GAD67 overexpression suppressed the elevation. Furthermore, the HDAd-DRG-GAD67-induced allodynia amelioration occurred even when we delayed intrathecal delivery of the therapeutic vector to day 7 after SNT.

conclusionHDAd-mediated DRG-targeted gene therapy delivering GAD67 is an efficacious treatment for neuropathic pain in SNT mice.

Indexed as

DRGGAD67Gene therapyHelper-dependent adenoviral vectorsHoming peptideNeuropathic pain

Identifiers

PMID30706038
PMCPMC6344132
OpenAlexW2896829913

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.