Evidence map›Paper›PMID 29255203›Full record

ArticleScientific reports2017

Growth Associated Protein 43 (GAP-43) as a Novel Target for the Diagnosis, Treatment and Prevention of Epileptogenesis.

Ashley D Nemes, Katayoun Ayasoufi, Zhong Ying, Qi-Gang Zhou, Hoonkyo Suh, Imad M Najm

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  6. GAP43 Located on Corticostriatal Terminals Restrains Novelty-Induced Hyperactivity in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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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

6 authors at 2 institutions in 1 country.

Ashley D NemesEpilepsy Center, Neurological Institute, Cleveland Clinic, 44195, Cleveland, OH, USA.
Katayoun AyasoufiDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Zhong YingEpilepsy Center, Neurological Institute, Cleveland Clinic, 44195, Cleveland, OH, USA.
Qi-Gang ZhouDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Hoonkyo SuhDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0002-4227-2982
Imad M NajmEpilepsy Center, Neurological Institute, Cleveland Clinic, 44195, Cleveland, OH, USA. najmi@ccf.org.
Cleveland Clinic · USCleveland Clinic Lerner College of Medicine · US

Funding

Alcohol-induced neurogenesisR01AA022377 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI SUH, HOONKYO · 2014 to 2018
$1.8M
NIAAA NIH HHS R01 AA022377
6 · The paper itself

Abstract

We previously showed increased growth associated protein 43 (GAP-43) expression in brain samples resected from patients with cortical dysplasia (CD), which was correlated with duration of epilepsy. Here, we used a rat model of CD to examine the regulation of GAP-43 in the brain and serum over the course of epileptogenesis. Baseline GAP-43 expression was higher in CD animals compared to control non-CD rats. An acute seizure increased GAP-43 expression in both CD and control rats. However, GAP-43 expression decreased by day 15 post-seizure in control rats, which did not develop spontaneous seizures. In contrast, GAP-43 remained up-regulated in CD rats, and over 50% developed chronic epilepsy with increased GAP-43 levels in their serum. GAP-43 protein was primarily located in excitatory neurons, suggesting its functional significance in epileptogenesis. Inhibition of GAP-43 expression by shRNA significantly reduced seizure duration and severity in CD rats after acute seizures with subsequent reduction in interictal spiking. Serum GAP-43 levels were significantly higher in CD rats that developed spontaneous seizures. Together, these results suggest GAP-43 as a key factor promoting epileptogenesis, a possible therapeutic target for treatment of progressive epilepsy and a potential biomarker for epilepsy progression in CD.

Indexed as

AnimalsBiomarkersDisease Models, AnimalElectroencephalographyEpilepsyGAP-43 ProteinGene Expression RegulationMaleMalformations of Cortical DevelopmentRatsRats, Sprague-DawleySeizuresBiomarkersGAP-43 Protein

Identifiers

PMID29255203
PMCPMC5735087
OpenAlexW2775041187

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.