Evidence map›Paper›PMID 39042667›Full record

ArticlePLoS biology2024

Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer's disease.

Rikesh M Rajani, Robert Ellingford, Mariam Hellmuth, Samuel S Harris, Orjona S Taso, David Graykowski, Francesca Kar Wey Lam, Charles Arber, Emre Fertan, John S H Danial and 9 more

Abstract read
In one paragraph

Article in PLoS biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

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  16. bioRxiv : the preprint server for biology · 2025
    Article
  17. Review
  18. Review
  19. Review
  20. Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Rikesh M RajaniUK Dementia Research Institute at UCL, University College London, London, United Kingdom.ORCID 0000-0003-3391-8654
Robert EllingfordUK Dementia Research Institute at UCL, University College London, London, United Kingdom.
Mariam HellmuthUK Dementia Research Institute at UCL, University College London, London, United Kingdom.
Samuel S HarrisUK Dementia Research Institute at UCL, University College London, London, United Kingdom.
Orjona S TasoUK Dementia Research Institute at UCL, University College London, London, United Kingdom.
David GraykowskiUK Dementia Research Institute at UCL, University College London, London, United Kingdom.
Francesca Kar Wey LamUK Dementia Research Institute at UCL, University College London, London, United Kingdom.
Charles ArberDepartment of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, United Kingdom.
Emre FertanYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, United Kingdom.
John S H DanialYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, United Kingdom.
Matthew SwireWolfson Institute for Biomedical Research, University College London, London, United Kingdom.
Marcus LloydWolfson Institute for Biomedical Research, University College London, London, United Kingdom.
Tatiana A GiovannucciDepartment of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, United Kingdom.
Mathieu BourdenxUK Dementia Research Institute at UCL, University College London, London, United Kingdom.
David KlenermanYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, United Kingdom.
Robert VassarDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States of America.
Selina WrayDepartment of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, United Kingdom.
Carlo Sala FrigerioUK Dementia Research Institute at UCL, University College London, London, United Kingdom.
Marc Aurel BuscheUK Dementia Research Institute at UCL, University College London, London, United Kingdom.ORCID 0000-0002-4416-7553

Funding

MRC MR/X019977/1UK Medical Research Council MR/X011038/1
6 · The paper itself

Abstract

Reduction of amyloid beta (Aβ) has been shown to be effective in treating Alzheimer's disease (AD), but the underlying assumption that neurons are the main source of pathogenic Aβ is untested. Here, we challenge this prevailing belief by demonstrating that oligodendrocytes are an important source of Aβ in the human brain and play a key role in promoting abnormal neuronal hyperactivity in an AD knock-in mouse model. We show that selectively suppressing oligodendrocyte Aβ production improves AD brain pathology and restores neuronal function in the mouse model in vivo. Our findings suggest that targeting oligodendrocyte Aβ production could be a promising therapeutic strategy for treating AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesDisease Models, AnimalMice, TransgenicNeuronsOligodendrogliaAmyloid beta-Protein PrecursorAnimalsBrainFemaleGene Knock-In TechniquesHumansMaleMiceAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAPP protein, humanAPP protein, mouse

Identifiers

PMID39042667
PMCPMC11265669

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.