Evidence map›Paper›PMID 37917233›Full record

ArticleJournal of neurology2024

Differential patterns of lysosomal dysfunction are seen in the clinicopathological forms of primary progressive aphasia.

Imogen J Swift, Simon Sjödin, Johan Gobom, Ann Brinkmalm, Kaj Blennow, Henrik Zetterberg, Jonathan D Rohrer, Aitana Sogorb-Esteve

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Endo-lysosomal dysfunction in neurodegenerative diseases: opinion on current progress and future direction in the use of exosomes as biomarkers.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
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

8 authors at 3 institutions in 2 countries.

Imogen J SwiftUK Dementia Research Institute at University College London, UCL Queen Square Institute of Neurology, University College London, London, UK.
Simon SjödinDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Johan GobomDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Ann BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergUK Dementia Research Institute at University College London, UCL Queen Square Institute of Neurology, University College London, London, UK.
Jonathan D RohrerUK Dementia Research Institute at University College London, UCL Queen Square Institute of Neurology, University College London, London, UK.
Aitana Sogorb-EsteveUK Dementia Research Institute at University College London, UCL Queen Square Institute of Neurology, University College London, London, UK. a.sogorb-esteve@ucl.ac.uk.ORCID http://orcid.org/0000-0002-7869-8192
Sahlgrenska University Hospital · SEUK Dementia Research Institute · GBUniversity of Gothenburg · SE

Funding

Medical Research Council MR/M008525/1Medical Research Council MR/M023664/1Medical Research Council MR/T046015/1
6 · The paper itself

Abstract

Increasing evidence implicates endo-lysosomal dysfunction in frontotemporal dementia (FTD). 18 proteins were quantified using a mass spectrometry assay panel in the cerebrospinal fluid of 36 people with the language variant of FTD, primary progressive aphasia (PPA) (including 13 with non-fluent variant (nfvPPA), 11 with semantic variant (svPPA), and 12 with logopenic variant (lvPPA)) and 19 healthy controls. The concentrations of the cathepsins (B, D, F, L1, and Z) as well as AP-2 complex subunit beta, ganglioside GM2 activator, beta-hexosaminidase subunit beta, tissue alpha L-fucosidase, and ubiquitin were decreased in nfvPPA compared with controls. In contrast, the concentrations of amyloid beta A4 protein, cathepsin Z, and dipeptidyl peptidase 2 were decreased in svPPA compared with controls. No proteins were abnormal in lvPPA. These results indicate a differential alteration of lysosomal proteins in the PPA variants, suggesting those with non-Alzheimer's pathologies are more likely to show abnormal lysosomal function.

Indexed as

Aphasia, Primary ProgressiveFrontotemporal DementiaAmyloid beta-PeptidesHumansLanguageLysosomesAmyloid beta-PeptidesEndo-lysosomal proteinsFrontotemporal dementiaPrimary progressive aphasiaUbiquitin

Identifiers

PMID37917233
PMCPMC10896779
OpenAlexW4388231690

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.