Evidence map›Paper›PMID 41957276›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026

Elimination of senescent cells fails to attenuate disease progression in an ALS mouse model.

Lisha Fang, Zhiyong Bai, Dong Yang, Bin Sun, Xudong Zhao, Jian Deng

Abstract read
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In one paragraph

Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Lisha FangDepartment of Targeting Therapy & Immunology and Laboratory of Cell Engineering and Immunotherapy, Cancer Center, State Key Laboratory of Respiratory Health and Multimorbidity and Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, No. 37 Guoxue Alley, Chengdu, Sichuan, 610041, China.
Zhiyong BaiDepartment of Targeting Therapy & Immunology and Laboratory of Cell Engineering and Immunotherapy, Cancer Center, State Key Laboratory of Respiratory Health and Multimorbidity and Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, No. 37 Guoxue Alley, Chengdu, Sichuan, 610041, China.
Dong YangDepartment of Targeting Therapy & Immunology and Laboratory of Cell Engineering and Immunotherapy, Cancer Center, State Key Laboratory of Respiratory Health and Multimorbidity and Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, No. 37 Guoxue Alley, Chengdu, Sichuan, 610041, China.
Bin SunShandong Provincial Key Laboratory of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Xudong ZhaoDepartment of Targeting Therapy & Immunology and Laboratory of Cell Engineering and Immunotherapy, Cancer Center, State Key Laboratory of Respiratory Health and Multimorbidity and Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, No. 37 Guoxue Alley, Chengdu, Sichuan, 610041, China.
Jian DengDepartment of Targeting Therapy & Immunology and Laboratory of Cell Engineering and Immunotherapy, Cancer Center, State Key Laboratory of Respiratory Health and Multimorbidity and Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, No. 37 Guoxue Alley, Chengdu, Sichuan, 610041, China. dengjian@stu.wchscu.cn.ORCID http://orcid.org/0000-0002-3947-9755

Funding

the Department of Science and Technology of Sichuan Province 2025NSFJQ0057
6 · The paper itself

Abstract

backgroundAmyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder involving progressive motor neuron degeneration, resulting in muscle weakness and paralysis. Current therapeutic options provide only modest benefit, and the etiology of ALS remains incompletely understood. Emerging evidence implicates cellular senescence in the central nervous system (CNS) of ALS pathogenesis, with senescent astrocytes identified in both animal models and patients.

methodsWe employed transgenic mice overexpressing the human superoxide dismutase 1 gene with a glycine-to-alanine substitution at codon 93 (hSOD1

resultsWe found that NKG2DLs

conclusionThese results indicate that while senescence is a pathogenic feature of ALS, it operates within an integrated disease network. Early senolytic intervention or combinatorial approaches may represent promising future strategies for ALS.

Indexed as

Amyotrophic Lateral SclerosisCellular SenescenceAnimalsDisease Models, AnimalDisease ProgressionHumansMiceMice, TransgenicNK Cell Lectin-Like Receptor Subfamily KSpinal CordSuperoxide Dismutase-1NK Cell Lectin-Like Receptor Subfamily KSOD1 protein, humanSuperoxide Dismutase-1Amyotrophic lateral sclerosisCellular senescenceNKG2D CAR-TSOD1G93A

Identifiers

PMID41957276

What OpenQuestion holds

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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.