Evidence map›Paper›PMID 39881195›Full record

ReviewNature neuroscience2025

Oligodendrocytes in Alzheimer's disease pathophysiology.

Shreeya Kedia, Mikael Simons

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing 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

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

  1. Pooled it
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  5. ENT1 inhibition links oligodendrocyte lipid metabolism to connectivity in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  10. When myelin breaks, tau aggregates - a new perspective on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
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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

2 authors.

Shreeya KediaInstitute of Neuronal Cell Biology, Technical University Munich, Munich, Germany.ORCID http://orcid.org/0000-0002-0445-1621
Mikael SimonsInstitute of Neuronal Cell Biology, Technical University Munich, Munich, Germany. mikael.simons@dzne.de.ORCID http://orcid.org/0000-0001-5329-192X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our understanding of Alzheimer's disease (AD) has transformed from a purely neuronal perspective to one that acknowledges the involvement of glial cells. Despite remarkable progress in unraveling the biology of microglia, astrocytes and vascular elements, the exploration of oligodendrocytes in AD is still in its early stages. Contrary to the traditional notion of oligodendrocytes as passive bystanders in AD pathology, emerging evidence indicates their active participation in and reaction to amyloid and tau pathology. Oligodendrocytes undergo a functional transition to a disease-associated state, engaging in immune modulation, stress responses and cellular survival. Far from being inert players, they appear to serve a dual role in AD pathogenesis, potentially offering defense mechanisms against pathology while also contributing to disease progression. This Review explores recent advancements in understanding the roles of oligodendrocytes and their myelin sheaths in the context of AD, shedding light on their complex interactions within the disease pathology.

Indexed as

Alzheimer DiseaseOligodendrogliaAnimalsHumansMyelin Sheath

Identifiers

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.