Evidence map›Paper›PMID 39390658›Full record

ArticleAnnals of neurology2024

Advanced MRI Measures of Myelin and Axon Volume Identify Repair in Multiple Sclerosis.

Gretel Sanabria-Diaz, Alessandro Cagol, Po-Jui Lu, Muhamed Barakovic, Mario Ocampo-Pineda, Xinjie Chen, Matthias Weigel, Esther Ruberte, Nina de Oliveira S Siebenborn, Riccardo Galbusera and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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

16 authors.

Gretel Sanabria-DiazNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-1595-7943
Alessandro CagolNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-7703-0553
Po-Jui LuNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0001-6031-6865
Muhamed BarakovicNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0001-8557-9223
Mario Ocampo-PinedaNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0003-2239-7355
Xinjie ChenNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.
Matthias WeigelNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-4910-1414
Esther RuberteNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-0195-4602
Nina de Oliveira S SiebenbornNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0009-0004-8810-2673
Riccardo GalbuseraNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-3092-8737
Sabine SchädelinNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-1150-0962
Pascal BenkertResearch Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0001-6525-8174
Jens KuhleNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-6963-8892
Ludwig KapposMultiple Sclerosis Centre, Department of Neurology, Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0003-4175-5509
Lester Melie-GarciaNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0001-5602-8916
Cristina GranzieraNeurology Clinic and Policlinic, Department of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-4917-8761

Funding

allgemeinen klinischen ForschungBiogenHorizon 2020 Eurostar program grant E!113682NovartisStiftung zur Förderung der gastroenterologischenSwiss National Science Foundation (SNSF) grant PP00P3_176984
6 · The paper itself

Abstract

objectivePathological studies suggest that multiple sclerosis (MS) lesions endure multiple waves of damage and repair; however, the dynamics and characteristics of these processes are poorly understood in patients living with MS.

methodsWe studied 128 MS patients (75 relapsing-remitting, 53 progressive) and 72 healthy controls who underwent advanced magnetic resonance imaging and clinical examination at baseline and 2 years later. Magnetization transfer saturation and multi-shell diffusion imaging were used to quantify longitudinal changes in myelin and axon volumes within MS lesions. Lesions were grouped into 4 classes (repair, damage, mixed repair damage, and stable). The frequency of each class was correlated to clinical measures, demographic characteristics, and levels of serum neurofilament light chain (sNfL).

resultsStable lesions were the most frequent (n = 2,276; 44%), followed by lesions with patterns of "repair" (n = 1,352; 26.2%) and damage (n = 1,214; 23.5%). The frequency of "repair" lesion was negatively associated with disability (β = -0.04; p < 0.001) and sNfL (β = -0.16; p < 0.001) at follow-up. The frequency of the "damage" class was higher in progressive than relapsing-remitting patients (p < 0.05) and was related to disability (baseline: β = -0.078; follow-up: β = -0.076; p < 0.001) and age (baseline: β = -0.078; p < 0.001). Stable lesions were more frequent in relapsing-remitting than in progressive patients (p < 0.05), and in younger patients versus older (β = -0.07; p < 0.001) at baseline. Further, "mixed" lesions were most frequent in older patients (β = 0.004; p < 0.001) at baseline.

interpretationThese findings show that repair and damage processes within MS lesions occur across the entire disease spectrum and that their frequency correlates with patients disability, age, disease duration, and extent of neuroaxonal damage. ANN NEUROL 2024.

Identifiers

PMID39390658
PMCPMC11683175

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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.