Evidence map›Paper›PMID 24638138›Full record

ReviewNature reviews. Neurology2014

Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis.

Manuel A Friese, Benjamin Schattling, Lars Fugger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 304 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
304citing papers in PubMed, 5 pooled it
37.6field-weighted citation impact, top 1% 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

304 citing papers in PubMed, 5 syntheses or guidelines pooled it, 620 citations in OpenAlex.

  1. Pooled it
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  6. Trial
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  13. Observational
  14. Review
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  16. Rethinking MS Therapeutics: From Disease Pathogenesis Mechanisms to AI-Driven Drug Discovery.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  17. Article
  18. Article
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244 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Manuel A FrieseZentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Falkenried 94, D-20251 Hamburg, Germany.
Benjamin SchattlingZentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Falkenried 94, D-20251 Hamburg, Germany.
Lars FuggerNuffield Department of Clinical Neurosciences and Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Universität Hamburg · DEMRC Human Immunology Unit · GB

Funding

Medical Research Council G1000800IWellcome Trust 100308
6 · The paper itself

Abstract

Multiple sclerosis (MS) is the most frequent chronic inflammatory disease of the CNS, and imposes major burdens on young lives. Great progress has been made in understanding and moderating the acute inflammatory components of MS, but the pathophysiological mechanisms of the concomitant neurodegeneration--which causes irreversible disability--are still not understood. Chronic inflammatory processes that continuously disturb neuroaxonal homeostasis drive neurodegeneration, so the clinical outcome probably depends on the balance of stressor load (inflammation) and any remaining capacity for neuronal self-protection. Hence, suitable drugs that promote the latter state are sorely needed. With the aim of identifying potential novel therapeutic targets in MS, we review research on the pathological mechanisms of neuroaxonal dysfunction and injury, such as altered ion channel activity, and the endogenous neuroprotective pathways that counteract oxidative stress and mitochondrial dysfunction. We focus on mechanisms inherent to neurons and their axons, which are separable from those acting on inflammatory responses and might, therefore, represent bona fide neuroprotective drug targets with the capability to halt MS progression.

Indexed as

AnimalsApoptosisAxonsBiomarkersHumansMultiple SclerosisNerve DegenerationSignal TransductionWallerian DegenerationBiomarkers

Identifiers

PMID24638138
OpenAlexW2051274614

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.