Evidence map›Paper›PMID 41396858›Full record

ReviewBrain : a journal of neurology2026

A cause and protective treatment for acute and progressive disability and grey matter atrophy.

Erika A Aguzzi, Roshni A Desai, Zhiyuan Yang, Andrew L Davies, Don Mahad, Bernard Siow, Ayse G Yenicelik, Radha Desai, Eleni Giama, AlBeshr Almasri and 5 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Brain : a journal of neurology, 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

15 authors.

Erika A AguzziDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
Roshni A DesaiDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
Zhiyuan YangDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
Andrew L DaviesDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
Don MahadCentre for Clinical Brain Sciences, University of Edinburgh, Edinburgh EH16 4SB, UK.
Bernard SiowIn Vivo Imaging, Biological Research Facility, The Francis Crick Institute, London NW1 1AT, UK.
Ayse G YenicelikDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
Radha DesaiDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
Eleni GiamaDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
AlBeshr AlmasriDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
Miranda ColmanDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.
Celine GeywitzDivision of Neuroimmunology, Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Mannheim 68167, Germany.
Lucas SchirmerDivision of Neuroimmunology, Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Mannheim 68167, Germany.ORCID 0000-0001-7142-4116
Paul A FeltsCentre for Anatomy and Human Identification, University of Dundee, Dundee DD1 4HN, UK.
Kenneth J SmithDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK.

Funding

Hertie Foundation P1180016
6 · The paper itself

Abstract

Acutely inflamed CNS lesions can be sufficiently hypoxic to cause temporary neurological disability. A new experimental lesion reveals that brief hypoxia can also ignite a slow-burning atrophy of the grey matter, resulting in a lifetime of slowly progressive disability. The progressive disability eventually exceeds that observed acutely, indicating that acutely functioning tissue can nevertheless be destined to atrophy. Remarkably, both the temporary initial disability and the ensuing progressive disability and atrophy are significantly reduced if the acute hypoxia is avoided by four days of treatment with vasodilating nimodipine, or by simply breathing raised oxygen concentration. Thus, a lifetime of progressive disability and neurodegeneration can be the legacy of a few days of inflammatory hypoxia experienced in young adulthood, and avoided by maintaining lesion oxygenation. The findings may help to understand and treat some progressive neurological disorders, including multiple sclerosis.

Indexed as

Gray MatterAnimalsAtrophyDisease ProgressionHumansMultiple Sclerosisdisease progressiongrey matter atrophyneurodegenerationneuroinflammationneuroprotectionrelapse

Identifiers

PMID41396858
PMCPMC13058463

What OpenQuestion holds

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Registered trials

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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.