Evidence map›Paper›PMID 40500505›Full record

ReviewAdvances in neurobiology2025

Protein Pathologies in Oligodendroglia in Neurodegenerative Diseases.

Shelley L Forrest, Gabor G Kovacs

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Shelley L ForrestTanz Centre for Research in Neurodegenerative Disease, University of Toronto, Toronto, ON, Canada.
Gabor G KovacsTanz Centre for Research in Neurodegenerative Disease, University of Toronto, Toronto, ON, Canada. gabor.kovacs@uhn.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases are clinically, pathologically and genetically heterogeneous disorders characterised by progressive dysfunction and neuronal loss and the deposition of disease-specific proteinaceous aggregates in neurons and/or glia, showing a hierarchical involvement of brain regions. Research into disease mechanisms underlying neurodegenerative disorders has focused on the proteinaceous neuronal aggregates in vulnerable brain regions leading to neuronal dysfunction and degeneration and onset of clinical symptoms. However, emerging evidence highlights the importance of glia, including oligodendroglia, in the pathogenesis of neurodegenerative diseases, which have been underappreciated and frequently considered secondary to neuronal involvement. Pathologically altered proteins depositing in oligodendroglia comprise phosphorylated tau, α-synuclein, transactive response DNA-binding protein-43 (TDP-43) and occasionally FET/FUS. However, only primary oligodendroglial tau and α-synuclein deposits are considered for neuropathological diagnosis and classification of some tauopathies and synucleinopathies, respectively. Oligodendroglial tau pathology is also seen in ageing-related tau oligodendrogliopathy (ARTOG). This chapter provides an overview of neurodegenerative proteinopathies and protein pathologies affecting oligodendroglia.

Indexed as

BrainNeurodegenerative DiseasesOligodendrogliaalpha-SynucleinAnimalsHumanstau Proteinsalpha-Synucleintau ProteinsNeurodegenerative diseaseOligodendrogliaTauTDP-43α-Synuclein

Identifiers

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.