Evidence map›Paper›PMID 37491450›Full record

ArticleScientific reports2023

Defects in early synaptic formation and neuronal function in Prader-Willi syndrome.

Shuhei Soeda, Daiki Ito, Tomoe Ogushi, Yui Sano, Ryosuke Negoro, Takuya Fujita, Ryo Saito, Hideo Taniura

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

8 authors at 2 institutions in 1 country.

Shuhei SoedaLaboratory of Neurochemistry, College of Pharmaceutical Sciences, Ritsumeikan University, 1-1-1 Noji Higashi, Kusatsu, Shiga, 525-8577, Japan. soeda05@fc.ritsumei.ac.jp.
Daiki ItoLaboratory of Neurochemistry, College of Pharmaceutical Sciences, Ritsumeikan University, 1-1-1 Noji Higashi, Kusatsu, Shiga, 525-8577, Japan.
Tomoe OgushiLaboratory of Neurochemistry, College of Pharmaceutical Sciences, Ritsumeikan University, 1-1-1 Noji Higashi, Kusatsu, Shiga, 525-8577, Japan.
Yui SanoLaboratory of Neurochemistry, College of Pharmaceutical Sciences, Ritsumeikan University, 1-1-1 Noji Higashi, Kusatsu, Shiga, 525-8577, Japan.
Ryosuke NegoroLaboratory of Molecular Pharmacokinetics, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga, 525-8577, Japan.
Takuya FujitaLaboratory of Molecular Pharmacokinetics, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga, 525-8577, Japan.
Ryo SaitoMitsubishi Tanabe Pharma Corporation, Kamoshida, Aoba, Yokohama, 227-0033, Japan.
Hideo TaniuraLaboratory of Neurochemistry, College of Pharmaceutical Sciences, Ritsumeikan University, 1-1-1 Noji Higashi, Kusatsu, Shiga, 525-8577, Japan.
Ritsumeikan University · JPMitsubishi Chemical (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prader-Willi syndrome (PWS), which is a complex epigenetic disorder caused by the deficiency of paternally expressed genes in chromosome 15q11-q13, is associated with several psychiatric dimensions, including autism spectrum disorder. We have previously reported that iPS cells derived from PWS patients exhibited aberrant differentiation and transcriptomic dysregulation in differentiated neural stem cells (NSCs) and neurons. Here, we identified SLITRK1 as a downregulated gene in NSCs differentiated from PWS patient iPS cells by RNA sequencing analysis. Because SLITRK1 is involved in synaptogenesis, we focused on the synaptic formation and function of neurons differentiated from PWS patient iPS cells and NDN or MAGEL2 single gene defect mutant iPS cells. Although βIII tubulin expression levels in all the neurons were comparable to the level of differentiation in the control, pre- and postsynaptic markers were significantly lower in PWS and mutant neurons than in control neurons. PSD-95 puncta along βIII tubulin neurites were also decreased. Membrane potential responses were measured while exposed to high K

Indexed as

Autism Spectrum DisorderNeural Stem CellsPrader-Willi SyndromeChromosomes, Human, Pair 15HumansIntracellular Signaling Peptides and ProteinsIntrinsically Disordered ProteinsNeuronsProteinsTubulinIntracellular Signaling Peptides and ProteinsIntrinsically Disordered ProteinsMAGEL2 protein, humanProteinsTubulin

Identifiers

PMID37491450
PMCPMC10368700
OpenAlexW4385236215

What Socratic 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 Socratic graph.