Evidence map›Paper›PMID 42320547›Full record

ArticleNeurobiology of disease2026

Proteomic analysis reveals early pathological defects in corticospinal motor neurons of a spastin model of hereditary spastic paraplegia, which are improved by NU-9 treatment.

Mukesh Gautam, Mercedes Priego, Christopher Quintanilla, Omar Kashow, Byoung-Kyu Cho, Young Ah Goo, Richard B Silverman, Gerardo Morfini, Peter W Baas, P Hande Ozdinler

Abstract read
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In one paragraph

Article in Neurobiology of disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Mukesh GautamDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Mercedes PriegoDepartment of Anatomy and Cell Biology, University of Illinois, Chicago, IL, USA.
Christopher QuintanillaDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Omar KashowDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Byoung-Kyu ChoMass Spectrometry Technology Access Center at the McDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO, USA; Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, USA.
Young Ah GooMass Spectrometry Technology Access Center at the McDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO, USA; Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO, USA.
Richard B SilvermanDepartment of Chemistry and Department of Molecular Biosciences, Northwestern University, 2145 Sheridan Road, Evanston, IL, USA; Department of Pharmacology, Feinberg School of Medicine, Chicago, IL 60611, USA; Chemistry of Life Processes Institute, Northwestern University, Evanston, IL 60208, USA.
Gerardo MorfiniDepartment of Anatomy and Cell Biology, University of Illinois, Chicago, IL, USA.
Peter W BaasDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA, USA.
P Hande OzdinlerDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA; Chemistry of Life Processes Institute, Northwestern University, Evanston, IL 60208, USA; Les Turner ALS Center, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA; Mesulam Institute for Cognitive Neurology and Alzheimer's Disease, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Electronic address: ozdinler@northwestern.edu.

Funding

Novel Protein Aggregation Inhibitors and Upper Motor Neuron Stabilizers for ALS and other Neurodegenerative DiseasesR01AG061708 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WILLIAM L KLEIN, Pembe Hande Ozdinler · 2019 to 2026
$10.5M
NIA NIH HHS R01 AG061708
6 · The paper itself

Abstract

Upper motor neuron (UMN) degeneration is a characteristic feature of hereditary spastic paraplegia (HSP), a genetically heterogeneous heritable neurodegenerative disorder resulting from mutations in over ninety genes. The mutations in the SPAST gene, which encodes the microtubule-severing protein spastin, are responsible for about 40% of all HSP cases. To date, the cellular and molecular mechanisms linking mutant spastin protein to UMN vulnerability in HSP patients remain unknown and there are no disease modifying therapies. To address this knowledge gap, we isolated pure populations of corticospinal motor neurons (CSMN; a.k.a. UMN in mice) from SPAST

Indexed as

Motor NeuronsSpastic Paraplegia, HereditarySpastinAnimalsDisease Models, AnimalMiceMice, TransgenicProteomeProteomicsProteomeSpastinSpast protein, mouseCSMNHSPNU-9SpastinUpper motor neurons

Identifiers

PMID42320547
PMCPMC13573564

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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.