Evidence map›Paper›PMID 41912527›Full record

ArticleNature communications2026

Targeting notch signaling to restore neural development and behavior in mouse models of ASD.

Yoko Hanno, Moe Nakanishi, Akinori Takase, Jun Nomura, Masami Tanaka, Yumi Iida, Masayuki Tanaka, Hiroyuki Hosokawa, Masatoshi Ito, Katsunaka Mikami and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. 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
–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

1 citing paper in PubMed.

  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

14 authors.

Yoko HannoDepartment of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan. yoko.hanno@riken.jp.ORCID http://orcid.org/0009-0006-2066-3276
Moe NakanishiRIKEN Center for Brain Science, Wako, Saitama, Japan.
Akinori TakaseThe Support Center for Medical Research and Education, Tokai University, Isehara, Kanagawa, Japan.
Jun NomuraDepartment of Physiology and Cell Biology, Kobe University School of Medicine, Chuo, Kobe, Japan.ORCID http://orcid.org/0000-0003-0817-2643
Masami TanakaDepartment of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.ORCID http://orcid.org/0000-0001-5782-0278
Yumi IidaThe Support Center for Medical Research and Education, Tokai University, Isehara, Kanagawa, Japan.
Masayuki TanakaThe Support Center for Medical Research and Education, Tokai University, Isehara, Kanagawa, Japan.ORCID http://orcid.org/0000-0002-8682-8719
Hiroyuki HosokawaDepartment of Immunology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.ORCID http://orcid.org/0000-0002-9592-2889
Masatoshi ItoDepartment of Legal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan.ORCID http://orcid.org/0000-0003-2665-0020
Katsunaka MikamiDepartment of Psychiatry, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Katsuto HozumiDepartment of Immunology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Goichi MiyoshiDepartment of Developmental Genetics and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Gunma, Japan.ORCID http://orcid.org/0000-0002-1872-6278
Toru TakumiRIKEN Center for Brain Science, Wako, Saitama, Japan.ORCID http://orcid.org/0000-0001-7153-266X
Takatoshi IijimaDepartment of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan. it1337@tokai.ac.jp.ORCID http://orcid.org/0009-0007-1841-3419

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) 15K14355MEXT | Japan Society for the Promotion of Science (JSPS) 20K22913MEXT | Japan Society for the Promotion of Science (JSPS) 21K07327MEXT | Japan Society for the Promotion of Science (JSPS) 24K10716
6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder with diverse genetic and environmental origins, yet whether these factors converge on common molecular pathways remains unclear. This study identifies dysregulation of the Notch signaling pathway as a shared mechanism in both hereditary and nonhereditary ASD models. Aberrant histone deacetylase 3-mediated epigenetic regulation of Notch signaling during embryonic forebrain development disrupts the specification of vasoactive intestinal peptide (VIP + ) GABAergic interneuron subtypes (VIP-INs), which originate in the caudal ganglionic eminence (CGE). CGE-specific ablation of Notch1/2 genes in ASD models restores the loss of VIP-INs, normalizes maladaptive excitatory and inhibitory balance, and selectively improves social behaviors. A single antenatal dose of a γ-secretase inhibitor ameliorates multiple ASD-associated neuronal, behavioral, and transcriptomic changes in adult models. The study indicates a strong convergence of ASD-related factors on Notch signaling dysregulation and establishes this pathway as a promising therapeutic target for developmental and behavioral deficits in ASD.

Indexed as

Autism Spectrum DisorderNeurogenesisReceptor, Notch1Receptor, Notch2Receptors, NotchAmyloid Precursor Protein SecretasesAnimalsBehavior, AnimalDisease Models, AnimalEpigenesis, GeneticFemaleGABAergic NeuronsGanglionic EminenceHumansInterneuronsMaleAmyloid Precursor Protein SecretasesNotch1 protein, mouseNotch2 protein, mouseReceptor, Notch1Receptor, Notch2Receptors, NotchVasoactive Intestinal Peptide

Identifiers

PMID41912527
PMCPMC13036009

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.