Evidence map›Paper›PMID 39443477›Full record

ArticleTranslational psychiatry2024

Soluble form of Lingo2, an autism spectrum disorder-associated molecule, functions as an excitatory synapse organizer in neurons.

Fumiaki Yoshida, Ryota Nagatomo, Shun Utsunomiya, Misaki Kimura, Shiyori Shun, Rena Kono, Yuma Kato, Yosuke Nao, Kazuma Maeda, Ryuta Koyama and 7 more

Abstract read
In one paragraph

Article in Translational psychiatry, 2024. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. 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

17 authors.

Fumiaki YoshidaLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Ryota NagatomoLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Shun UtsunomiyaNeuroscience 2, Laboratory for Drug Discovery and Disease Research, Shionogi & Co. Ltd, Osaka, Japan.
Misaki KimuraLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Shiyori ShunLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Rena KonoLaboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Yuma KatoLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Yosuke NaoLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Kazuma MaedaNeuroscience 2, Laboratory for Drug Discovery and Disease Research, Shionogi & Co. Ltd, Osaka, Japan.
Ryuta KoyamaLaboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Yuji IkegayaLaboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Stefan F LichtenthalerGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.ORCID 0000-0003-2211-2575
Sho TakatoriLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-3925-4011
Hiroshi TakemotoNeuroscience 2, Laboratory for Drug Discovery and Disease Research, Shionogi & Co. Ltd, Osaka, Japan.ORCID 0000-0001-9893-0609
Koichi OgawaNeuroscience 2, Laboratory for Drug Discovery and Disease Research, Shionogi & Co. Ltd, Osaka, Japan.
Genta ItoDepartment of Biomolecular Chemistry, Faculty of Pharma-Science, Teikyo University, Tokyo, Japan.ORCID 0000-0001-6370-1099
Taisuke TomitaLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan. taisuke@mol.f.u-tokyo.ac.jp.ORCID 0000-0002-0075-5943

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 390857198Japan Agency for Medical Research and Development (AMED) 22g1510002h0002MEXT | Japan Science and Technology Agency (JST) JPMJER1801MEXT | Japan Society for the Promotion of Science (JSPS) 15H02492MEXT | Japan Society for the Promotion of Science (JSPS) 19H01015MEXT | Japan Society for the Promotion of Science (JSPS) 19J14908MEXT | Japan Society for the Promotion of Science (JSPS) 20K21471MEXT | Japan Society for the Promotion of Science (JSPS) 22K21353MEXT | Japan Society for the Promotion of Science (JSPS) 23H00394
6 · The paper itself

Abstract

Autism Spectrum Disorder (ASD) is a developmental disorder characterized by impaired social communication and repetitive behaviors. In recent years, a pharmacological mouse model of ASD involving maternal administration of valproic acid (VPA) has become widely used. Newborn pups in this model show an abnormal balance between excitatory and inhibitory (E/I) signaling in neurons and exhibit ASD-like behavior. However, the molecular basis of this model and its implications for the pathogenesis of ASD in humans remain unknown. Using quantitative secretome analysis, we found that the level of leucine-rich repeat and immunoglobulin domain-containing protein 2 (Lingo2) was upregulated in the conditioned medium of VPA model neurons. This upregulation was associated with excitatory synaptic organizer activity. The secreted form of the extracellular domain of Lingo2 (sLingo2) is produced by the transmembrane metalloprotease ADAM10 through proteolytic processing. sLingo2 was found to induce the formation of excitatory synapses in both mouse and human neurons, and treatment with sLingo2 resulted in an increased frequency of miniature excitatory postsynaptic currents in human neurons. These findings suggest that sLingo2 is an excitatory synapse organizer involved in ASD, and further understanding of the mechanisms by which sLingo2 induces excitatory synaptogenesis is expected to advance our understanding of the pathogenesis of ASD.

Indexed as

Autism Spectrum DisorderDisease Models, AnimalMembrane ProteinsNerve Tissue ProteinsNeuronsSynapsesADAM10 ProteinAnimalsExcitatory Postsynaptic PotentialsFemaleHumansMiceMice, Inbred C57BLValproic AcidADAM10 ProteinLingo2 protein, mouseMembrane ProteinsNerve Tissue ProteinsValproic Acid

Identifiers

PMID39443477
PMCPMC11500186

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.