Evidence map›Paper›PMID 36323511›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2023

Senescent-like Blood Lymphocytes and Disease Progression in Amyotrophic Lateral Sclerosis.

Ozlem Yildiz, Johannes Schroth, Timothy Tree, Martin R Turner, Pamela J Shaw, Sian M Henson, Andrea Malaspina

Open access · goldAbstract read
In one paragraph

Article in Neurology(R) neuroimmunology & neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
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

28 citing papers in PubMed, 31 citations in OpenAlex.

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  20. The presence and clinical significance of autoantibodies in amyotrophic lateral sclerosis: a narrative review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
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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

7 authors at 4 institutions in 1 country.

Ozlem YildizFrom the Neuroscience and Trauma Centre (O.Y., A.M.), Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London; Queen Square Motor Neuron Disease Centre (A.M.), Neuromuscular Department, Institute of Neurology, University College London; Translational Medicine and Therapeutics (J.S., S.M.H.), William Harvey Research Institute, Barts and the London, Queen Mary University of London; Department of Immunobiology (T.T.), School of Immunology & Microbial Sciences, King's College London; Nuffield Department of Clinical Neurosciences (M.R.T.), University of Oxford; and Sheffield Institute for Translational Neuroscience (P.J.S.), University of Sheffield, UK.
Johannes SchrothFrom the Neuroscience and Trauma Centre (O.Y., A.M.), Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London; Queen Square Motor Neuron Disease Centre (A.M.), Neuromuscular Department, Institute of Neurology, University College London; Translational Medicine and Therapeutics (J.S., S.M.H.), William Harvey Research Institute, Barts and the London, Queen Mary University of London; Department of Immunobiology (T.T.), School of Immunology & Microbial Sciences, King's College London; Nuffield Department of Clinical Neurosciences (M.R.T.), University of Oxford; and Sheffield Institute for Translational Neuroscience (P.J.S.), University of Sheffield, UK.
Timothy TreeFrom the Neuroscience and Trauma Centre (O.Y., A.M.), Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London; Queen Square Motor Neuron Disease Centre (A.M.), Neuromuscular Department, Institute of Neurology, University College London; Translational Medicine and Therapeutics (J.S., S.M.H.), William Harvey Research Institute, Barts and the London, Queen Mary University of London; Department of Immunobiology (T.T.), School of Immunology & Microbial Sciences, King's College London; Nuffield Department of Clinical Neurosciences (M.R.T.), University of Oxford; and Sheffield Institute for Translational Neuroscience (P.J.S.), University of Sheffield, UK.
Martin R TurnerFrom the Neuroscience and Trauma Centre (O.Y., A.M.), Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London; Queen Square Motor Neuron Disease Centre (A.M.), Neuromuscular Department, Institute of Neurology, University College London; Translational Medicine and Therapeutics (J.S., S.M.H.), William Harvey Research Institute, Barts and the London, Queen Mary University of London; Department of Immunobiology (T.T.), School of Immunology & Microbial Sciences, King's College London; Nuffield Department of Clinical Neurosciences (M.R.T.), University of Oxford; and Sheffield Institute for Translational Neuroscience (P.J.S.), University of Sheffield, UK.
Pamela J ShawFrom the Neuroscience and Trauma Centre (O.Y., A.M.), Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London; Queen Square Motor Neuron Disease Centre (A.M.), Neuromuscular Department, Institute of Neurology, University College London; Translational Medicine and Therapeutics (J.S., S.M.H.), William Harvey Research Institute, Barts and the London, Queen Mary University of London; Department of Immunobiology (T.T.), School of Immunology & Microbial Sciences, King's College London; Nuffield Department of Clinical Neurosciences (M.R.T.), University of Oxford; and Sheffield Institute for Translational Neuroscience (P.J.S.), University of Sheffield, UK.
Sian M HensonFrom the Neuroscience and Trauma Centre (O.Y., A.M.), Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London; Queen Square Motor Neuron Disease Centre (A.M.), Neuromuscular Department, Institute of Neurology, University College London; Translational Medicine and Therapeutics (J.S., S.M.H.), William Harvey Research Institute, Barts and the London, Queen Mary University of London; Department of Immunobiology (T.T.), School of Immunology & Microbial Sciences, King's College London; Nuffield Department of Clinical Neurosciences (M.R.T.), University of Oxford; and Sheffield Institute for Translational Neuroscience (P.J.S.), University of Sheffield, UK.
Andrea MalaspinaFrom the Neuroscience and Trauma Centre (O.Y., A.M.), Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London; Queen Square Motor Neuron Disease Centre (A.M.), Neuromuscular Department, Institute of Neurology, University College London; Translational Medicine and Therapeutics (J.S., S.M.H.), William Harvey Research Institute, Barts and the London, Queen Mary University of London; Department of Immunobiology (T.T.), School of Immunology & Microbial Sciences, King's College London; Nuffield Department of Clinical Neurosciences (M.R.T.), University of Oxford; and Sheffield Institute for Translational Neuroscience (P.J.S.), University of Sheffield, UK. a.malaspina@ucl.ac.uk.
University College London · GBKing's College London · GBQueen Mary University of London · GBWilliam Harvey Research Institute · GB

Funding

Department of Health BRC-1215-20017Department of Health NF-SI-0617-10077Motor Neurone Disease Association TURNER/OCT15/972-797Motor Neurone Disease Association TURNER/OCT18/989-797
6 · The paper itself

Abstract

BACKGROUND AND

objectivesAging is known to exacerbate neuroinflammation, and in the neurodegenerative disorder amyotrophic lateral sclerosis (ALS), an older age is associated with a worse prognosis. We have previously shown the activation of cell senescence pathways in the proteome of peripheral blood mononuclear cells and the increase of proinflammatory cytokines in blood from individuals living with ALS. In this single-center, retrospective study, we investigated the expression of senescent-like blood mononuclear cells in ALS.

methodsWe first applied multidimensional cytometry by time-of-flight (CyTOF) to study the senescent immunophenotype of blood mononuclear cells from 21 patients with ALS and 10 healthy controls (HCs). We then used targeted flow cytometry (FC) to investigate frequencies of senescent blood lymphocytes in 40 patients with ALS and 20 HCs. Longitudinal analysis included 2 additional time points in 17 patients with ALS. Frequencies of senescent-like lymphocytes were analyzed in relation to survival.

resultsUnsupervised clustering of CyTOF data showed higher frequencies of senescent CD4 DISCUSSION: Our data suggest that a systemic elevation of senescent and late memory T and B lymphocytes is a feature of faster progressing ALS and of ALS individuals with bulbar involvement. Lymphocyte senescence and their memory state may be central to the immune dysregulation known to drive disease progression in ALS and a target for biomarkers and therapeutics discovery.

Indexed as

Amyotrophic Lateral SclerosisCD4-Positive T-LymphocytesDisease ProgressionHumansLeukocytes, MononuclearRetrospective Studies

Identifiers

PMID36323511
PMCPMC9673751
OpenAlexW4308135426

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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.