Evidence map›Paper›PMID 41218062›Full record

ArticleBrain : a journal of neurology2026

Single-nucleus multiome shows motor neuron glutamate overactivation in amyotrophic lateral sclerosis.

Eriko Takeuchi, Yoshiaki Yasumizu, Junko Morita, Masakazu Ishikawa, Kotaro Ogawa, Daisuke Motooka, Daisuke Okuzaki, Miho Nagata, Yasuki Ishihara, Yohei Miyashita and 8 more

Abstract read
In one paragraph

Article in Brain : a journal of neurology, 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

18 authors.

Eriko TakeuchiDepartment of Neurology, The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Yoshiaki YasumizuDepartment of Neurology, The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.ORCID 0000-0002-9872-4909
Junko MoritaDepartment of Neurotherapeutics, The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Masakazu IshikawaGenome Information Research Center, The University of Osaka, Suita, Osaka 565-0871, Japan.
Kotaro OgawaDepartment of Neurology, The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Daisuke MotookaIntegrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), The University of Osaka, Suita, Osaka 565-0871, Japan.
Daisuke OkuzakiIntegrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), The University of Osaka, Suita, Osaka 565-0871, Japan.ORCID 0000-0002-4552-783X
Miho NagataDepartment of Cardiovascular Medicine (IRUD Analysis Center), The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Yasuki IshiharaDepartment of Cardiovascular Medicine (IRUD Analysis Center), The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Yohei MiyashitaDepartment of Cardiovascular Medicine (IRUD Analysis Center), The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Yoshihiro AsanoDepartment of Cardiovascular Medicine (IRUD Analysis Center), The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Kohji MoriDepartment of Psychiatry, The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Eiichi MoriiIntegrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), The University of Osaka, Suita, Osaka 565-0871, Japan.
Goichi BeckDepartment of Neurology, The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Yuko SaitoDepartment of Neuropathology (Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Itabashi, Tokyo 173-0015, Japan.
Shigeo MurayamaBrain Bank for Neurodevelopmental, Molecular Research Center for Children's Mental Development, Neurological and Psychiatric Disorders, The University of Osaka United Graduate School of Child Development, Suita, Osaka 565-0871, Japan.ORCID 0000-0001-9709-5242
Hideki MochizukiDepartment of Neurology, The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.ORCID 0000-0002-0874-7542
Seiichi NaganoDepartment of Neurology, The University of Osaka Graduate School of Medicine, Suita, Osaka 565-0871, Japan.

Funding

AMED JP20lm0203007AMED JP21ek0109520AMED JP21wm0525029Institute for Open and Transdisciplinary Research InitiativesIntegrated Frontier Research for Medical Science DivisionJSPS KAKENHI JP21H02841JSPS KAKENHI JP22H04811JSPS KAKENHI JP23K18265JSPS KAKENHI JP24K02370Osaka UniversityResearch Institute for Microbial Diseases
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that causes motor neuron degeneration. However, the mechanisms underlying the selective vulnerability of motor neurons and the involvement of non-motor neuron cells in ALS remain unclear. To investigate ALS pathology at the cellular level, we performed a single-nucleus multiome analysis, including RNA sequencing and chromatin accessibility profiling, on the motor cortex (75 583 nuclei) and spinal cord (62 711 nuclei) from patients with ALS (n = 6) and controls (n = 6). Our results revealed significant gene expression changes specifically in spinal motor neurons, including upregulation of a metabotropic glutamate receptor, GRM5, and enhanced glutamate signalling. By integrating genome-wide association study data, we identified ALS-associated single nucleotide polymorphisms (SNPs) in regulatory regions, suggesting cell-type-specific enrichment of risk, especially in microglia. These findings suggest that changes in spinal motor neurons and their surrounding environment, including glutamate signalling, may be involved in ALS pathology. The study also provides valuable resources for future research on the underlying mechanisms and potential therapeutic targets.

Indexed as

Amyotrophic Lateral SclerosisGlutamic AcidMotor NeuronsAgedFemaleGenome-Wide Association StudyHumansMaleMiddle AgedMotor CortexPolymorphism, Single NucleotideSpinal CordGlutamic Acidamyotrophic lateral sclerosisGWASmotor cortexsingle nucleus ATAC-seqsingle nucleus RNA-seqspinal cord

Identifiers

PMID41218062
PMCPMC13337230

What OpenQuestion holds

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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 OpenQuestion graph.