OSCR

Topological modeling of gene expression in the brain with Huntington's disease reveals selective disruption of co-expression network.

Overview

Authors: Yuko Okamura-Oho1,2, Kazuro Shimokawa3, Satoshi Oota1,4, Atsushi Yoshiki4, Masahiko Morita1, Masaomi Nishimura1, Sakiko Nakamura1, Yuki Tsujimura1, Shumpei Ishikawa3, Hideo Yokota1
  1. RIKEN Center for Advanced Photonics, Wako, 351-0198 Saitama Japan
  2. Faculty of Food Sciences and Nutrition, Jissen Women’s University, Hino, 191- 8510 Tokyo Japan
  3. Department of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033 Japan
  4. RIKEN Bioresource Research Center, Tsukuba, Ibaraki Japan
Journal: Scientific reports, volume 16, issue 1, article 18328
Dates: received 14 November 2025; accepted 28 May 2026; published online 30 June 2026
Type: Research article · Language: English
License: CC BY-NC-ND
Identifiers: DOI 10.1038/s41598-026-56101-8 · PMID 42380167 · PMCID PMC13319467 · OpenAlex W7166670214
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: genetics / omics (modality), human (organism), mouse (organism), other condition (population), cellular / molecular (subfield)
Methods: Connectivity
Keywords: Computational biology and bioinformatics, Genetics, Molecular biology, Neurology, Neuroscience
MeSH: Brain*, Gene Expression Regulation*, Gene Regulatory Networks*, Huntington Disease*, Animals, Brain-Derived Neurotrophic Factor, Disease Models, Animal, DNA Helicases, Gene Expression Profiling, Humans, Huntingtin Protein, LIM-Homeodomain Proteins, Medium Spiny Neurons, Mice, Mice, Transgenic, Nerve Tissue Proteins, Nuclear Proteins, Transcription Factors (* major topic)
Topic: Genetic Neurodegenerative Diseases (Cellular and Molecular Neuroscience, Neuroscience), according to OpenAlex
Funding: Japan Society for the Promotion of Science (25560428, 26280110, 268032, 15HP8038, 16HP8032, and 17HP8082, JP15H05954)
Citations: not cited yet (Europe PMC); 50 references in the paper

Abstract

The abstract is not reproduced here: the paper's license (CC BY-NC-ND) does not allow it. Read it in the paper, at the publisher or on Europe PMC.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

Data availability statement

The paper has a data availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:

Read it in the paper: doi.org/10.1038/s41598-026-56101-8.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 10 authors, 5 keywords, 18 MeSH terms, 1 funder, 50 references.

Cite

This paper

Okamura-Oho, Y., Shimokawa, K., Oota, S., Yoshiki, A., Morita, M., Nishimura, M., Nakamura, S., Tsujimura, Y., Ishikawa, S., & Yokota, H. (2026). Topological modeling of gene expression in the brain with Huntington's disease reveals selective disruption of co-expression network. Scientific reports, 16(1), 18328. https://doi.org/10.1038/s41598-026-56101-8

BibTeX

@article{okamuraoho2026topological,
author = {Okamura-Oho, Yuko and Shimokawa, Kazuro and Oota, Satoshi and Yoshiki, Atsushi and Morita, Masahiko and Nishimura, Masaomi and Nakamura, Sakiko and Tsujimura, Yuki and Ishikawa, Shumpei and Yokota, Hideo},
title = {{Topological modeling of gene expression in the brain with Huntington's disease reveals selective disruption of co-expression network}},
journal = {Scientific reports},
year = {2026},
month = jun,
volume = {16},
number = {1},
pages = {18328},
publisher = {Nature Publishing Group},
issn = {2045-2322},
doi = {10.1038/s41598-026-56101-8},
url = {https://doi.org/10.1038/s41598-026-56101-8},
pmid = {42380167},
pmcid = {PMC13319467}
}

RIS

TY - JOUR
AU - Okamura-Oho, Yuko
AU - Shimokawa, Kazuro
AU - Oota, Satoshi
AU - Yoshiki, Atsushi
AU - Morita, Masahiko
AU - Nishimura, Masaomi
AU - Nakamura, Sakiko
AU - Tsujimura, Yuki
AU - Ishikawa, Shumpei
AU - Yokota, Hideo
TI - Topological modeling of gene expression in the brain with Huntington's disease reveals selective disruption of co-expression network
T2 - Scientific reports
J2 - Sci Rep
PY - 2026
DA - 2026/06/30
VL - 16
IS - 1
SP - 18328
SN - 2045-2322
PB - Nature Publishing Group
DO - 10.1038/s41598-026-56101-8
UR - https://doi.org/10.1038/s41598-026-56101-8
LA - en
ER -

CSL-JSON

{
"id": "10.1038/s41598-026-56101-8",
"type": "article-journal",
"title": "Topological modeling of gene expression in the brain with Huntington's disease reveals selective disruption of co-expression network",
"container-title": "Scientific reports",
"author": [
{
"family": "Okamura-Oho",
"given": "Yuko"
},
{
"family": "Shimokawa",
"given": "Kazuro"
},
{
"family": "Oota",
"given": "Satoshi"
},
{
"family": "Yoshiki",
"given": "Atsushi"
},
{
"family": "Morita",
"given": "Masahiko"
},
{
"family": "Nishimura",
"given": "Masaomi"
},
{
"family": "Nakamura",
"given": "Sakiko"
},
{
"family": "Tsujimura",
"given": "Yuki"
},
{
"family": "Ishikawa",
"given": "Shumpei"
},
{
"family": "Yokota",
"given": "Hideo"
}
],
"container-title-short": "Sci Rep",
"volume": "16",
"issue": "1",
"page": "18328",
"DOI": "10.1038/s41598-026-56101-8",
"PMID": "42380167",
"PMCID": "PMC13319467",
"ISSN": "2045-2322",
"publisher": "Nature Publishing Group",
"URL": "https://doi.org/10.1038/s41598-026-56101-8",
"language": "en",
"issued": {
"date-parts": [
[
2026,
6,
30
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1242/dmm.052803
Molecular features of a Huntington's disease knock-in minipig.
Journal: Disease models & mechanisms
In common: other condition, cellular / molecular, 3 references
[2] doi:10.1186/s13024-026-00960-2 [code]
Temporal single-cell atlas of full-length Huntington's disease mouse model defines stage-specific signatures of corticostriatal dysfunction.
Journal: Molecular neurodegeneration
In common: genetics / omics, other condition, mouse, 2 references
[3] doi:10.1177/18796397261443137 [code]
Towards AI-driven prediction of <i>HTT</i> CAG size in super-expanded human spiny projection neurons from Huntington disease donors.
Journal: Journal of Huntington's disease
In common: genetics / omics, other condition, cellular / molecular, 2 references
[4] doi:10.1038/s44321-026-00459-9
Anle138b ameliorates pathological phenotypes in mouse and cellular models of Huntington's disease.
Journal: EMBO molecular medicine
In common: other condition, mouse, cellular / molecular, 2 references
[5] doi:10.1038/s41586-026-10671-9 [code]
Restoring cortical disinhibition improves Huntington's disease phenotypes.
Journal: Nature
In common: other condition, mouse, 2 references
[6] doi:10.1007/s12035-026-05973-y
Integrative Transcriptomic, Network, and Machine Learning Analyses Identify Genistein and Resveratrol-Associated Therapeutic Targets in Alzheimer's Disease.
Journal: Molecular neurobiology
In common: genetics / omics, cellular / molecular, 2 references
[7] doi:10.1007/s10571-026-01726-6
Gene Expression Analysis of Mitochondria-Associated Membrane (MAM)-Related Genes in ER Stress and Alzheimer's Disease.
Journal: Cellular and molecular neurobiology
In common: genetics / omics, cellular / molecular, 2 references
[8] doi:10.3390/ijms27177675
LncRNA Gas5, a Target of the Nonsense-Mediated Decay Pathway in the Brain, Regulates Neuroinflammation and Neurodegenerative Disease Pathways in a Tauopathy Mouse Model.
Journal: International journal of molecular sciences
In common: genetics / omics, other condition, mouse, 1 other category, 1 reference
[9] doi:10.1371/journal.ppat.1014115 [code]
Venezuelan equine encephalitis virus infection causes chronic neurobehavioral outcomes, cellular remodeling, and hippocampal single-cell transcriptomic changes.
Journal: PLoS pathogens
In common: genetics / omics, other condition, mouse, 1 other category, 1 reference
[10] doi:10.1038/s41598-026-54412-4 [code]
Single-cell transcriptomics and mouse model phenotyping for biomarker screen of peripheral blood in Huntington's disease.
Journal: Scientific reports
In common: genetics / omics, other condition, mouse, 1 reference

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.