Evidence map›Paper›PMID 36847937›Full record

ArticleMolecular neurobiology2023

Insulin-Like Growth Factor-1 Promotes Synaptogenesis Signaling, a Major Dysregulated Pathway in Malformation of Cortical Development, in a Rat Model.

Minyoung Lee, Eun-Jin Kim, Min-Jee Kim, Mi-Sun Yum, Jeonghun Yeom, Kyunggon Kim

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. 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

6 authors at 2 institutions in 1 country.

Minyoung LeeDepartment of Pediatrics, University of Ulsan College of Medicine, Seoul, 05505, South Korea.ORCID http://orcid.org/0000-0001-6636-6054
Eun-Jin KimDepartment of Pediatrics, University of Ulsan College of Medicine, Seoul, 05505, South Korea.
Min-Jee KimDepartment of Pediatrics, Asan Medical Center Children's Hospital, 88 Olympic-ro, Songpa-ku, 05505, Seoul, South Korea.
Mi-Sun YumDepartment of Pediatrics, University of Ulsan College of Medicine, Seoul, 05505, South Korea. misun.yum@gmail.com.ORCID http://orcid.org/0000-0002-5986-5258
Jeonghun YeomDepartment of Convergence Medicine, Asan Medical Center, University of Ulsan, 05505, Seoul, South Korea.
Kyunggon KimAsan Institute for Life Sciences, Asan Medical Center, Seoul, 05505, South Korea.
Asan Medical Center · KRUlsan College · KR

Funding

National Research Foundation of Korea NRF-2019R1A6A3A01090600National Research Foundation of Korea NRF-2021R1A2C100447111
6 · The paper itself

Abstract

Malformation of cortical development (MCD) is one of the main causes of intractable epilepsy in childhood. We explored a treatment based on molecular changes using an infant rat model of methylazoxymethanol (MAM)-induced MCD established by injecting MAM at gestational day 15. The offspring were sacrificed on postnatal day (P) 15 for proteomic analysis, which revealed significant downregulation in the synaptogenesis signaling pathway in the cortex of MCD rats. Recombinant human insulin-growth factor-1 (rhIGF-1) was injected from P12 to P14 twice daily and the effect of IGF1 on N-methyl-D-aspartate (NMDA)-induced spasms (15 mg/kg of NMDA, i.p.) was tested; the onset of P15 single spasm was significantly delayed (p = 0.002) and the number of spasms decreased (p < 0.001) in rhIGF1-pretreated rats (n = 17) compared to those in VEH-treated rats (n = 18). Electroencephalographic monitoring during spasms showed significantly reduced spectral entropy and event-related spectral dynamics of fast oscillation in rhIGF-1 treated rats. Magnetic resonance spectroscopy of the retrosplenial cortex showed decreased glutathione (GSH) (p = 0.039) and significant developmental changes in GSH, phosphocreatine (PCr), and total creatine (tCr) (p = 0.023, 0.042, 0.015, respectively) after rhIGF1 pretreatment. rhIGF1 pretreatment significantly upregulated expression of cortical synaptic proteins such as PSD95, AMPAR1, AMPAR4, NMDAR1, and NMDAR2A (p < 0.05). Thus, early rhIGF-1 treatment could promote synaptic protein expression, which was significantly downregulated by prenatal MAM exposure, and effectively suppress NMDA-induced spasms. Early IGF1 treatment should be further investigated as a therapeutic strategy in infants with MCD-related epilepsy.

Indexed as

EpilepsyN-MethylaspartateAnimalsDisease Models, AnimalFemaleHumansInfantInsulin-Like Growth Factor IMethylazoxymethanol AcetatePregnancyProteomicsRatsSpasmInsulin-Like Growth Factor ImethylazoxymethanolMethylazoxymethanol AcetateN-MethylaspartateAnimal modelMalformation of cortical development (MCD)Methylazoxymethanol acetate (MAM)Recombinant human insulin-like growth factor-1 (rhIGF-1)Synaptic protein

Identifiers

PMID36847937
OpenAlexW4322496530

What OpenQuestion holds

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Read underepoch 390

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.