Evidence map›Paper›PMID 41028049›Full record

ArticleScientific reports2025

Proteomic analysis of brain and spinal cord tissue reveals distinct immune and mitochondrial processes between human and mouse ALS models.

Alanna G Spiteri, Joel R Steele, Han-Chung Lee, Haijian Zhang, Jiaqi Sun, Ralf B Schittenhelm, Chien-Hsiung Yu, Catriona McLean, Colin L Masters, Benjamin Goudey and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. 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

12 authors.

Alanna G SpiteriThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia. spiteri.alanna@gmail.com.
Joel R SteeleMonash Proteomics and Metabolomics Platform, Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC, 3168, Australia.
Han-Chung LeeMonash Proteomics and Metabolomics Platform, Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC, 3168, Australia.
Haijian ZhangMonash Proteomics and Metabolomics Platform, Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC, 3168, Australia.
Jiaqi SunThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
Ralf B SchittenhelmMonash Proteomics and Metabolomics Platform, Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC, 3168, Australia.
Chien-Hsiung YuThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
Catriona McLeanFlorey Department of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, 3052, Australia.
Colin L MastersThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
Benjamin GoudeyFlorey Department of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, 3052, Australia.
Liang JinThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia. liang.jin@monash.edu.
Yijun PanThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia. yijun.pan@monash.edu.

Funding

Alzheimer's Association grant AARF1020292National Health and Medical Research Council GNT2007912NHMRC-AMED 2022 Dementia Collaborative Research GNT2022203
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease resulting in the progressive loss of motor neurons in the brain and spine. More than 95% of cases are pathologically characterized by the cytoplasmic accumulation of hyperphosphorylated and ubiquitinated transactive response DNA-binding protein 43 (TDP-43). Multiple mouse models with TDP-43 accumulation have been developed, however, whether they recapitulate molecular features of ALS pathology is unclear. Given the lack of curative treatment for ALS, there is an urgent need to identify the precise biological processes contributing to disease pathogenesis for the development of effective therapeutic treatments. Thus, in this study we employed label-based untargeted proteomics to characterize the ALS proteome and related biological processes in the spinal cord and brain of TDP-43

Indexed as

Amyotrophic Lateral SclerosisBrainMitochondriaProteomeProteomicsSpinal CordAnimalsDisease Models, AnimalDNA-Binding ProteinsFemaleHumansMaleMiceMice, TransgenicMotor NeuronsDNA-Binding ProteinsProteomeTARDBP protein, humanAmyotrophic lateral sclerosisImmune-mediated pathologyMitochondrial dysfunctionMotor neurone diseaseNeurodegenerationTMT-proteomics

Identifiers

PMID41028049
PMCPMC12484661

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Registered trials

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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.