Evidence map›Paper›PMID 38970706›Full record

ArticleMolecular and cellular biochemistry2025

Lack of cellular prion protein causes Amyloid β accumulation, increased extracellular vesicle abundance, and changes to exosome biogenesis proteins.

Lovisa Johansson, Juan F Reyes, Tahir Ali, Hermann Schätzl, Sabine Gilch, Martin Hallbeck

Abstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Unlocking the potential of extracellular vesicles in cancer diagnosis and therapy: a comprehensive bibliometric study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Review
  3. 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

6 authors.

Lovisa JohanssonDepartment of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, Linköping, Sweden. Lovisa.Johansson@liu.se.
Juan F ReyesDepartment of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, Linköping, Sweden.
Tahir AliCalgary Prion Research Unit, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada.
Hermann SchätzlCalgary Prion Research Unit, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada.
Sabine GilchCalgary Prion Research Unit, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada.
Martin HallbeckDepartment of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, Linköping, Sweden. Martin.Hallbeck@liu.se.

Funding

Vetenskapsrådet 2019-01016
6 · The paper itself

Abstract

Alzheimer's disease (AD) progression is closely linked to the propagation of pathological Amyloid β (Aβ), a process increasingly understood to involve extracellular vesicles (EVs), namely exosomes. The specifics of Aβ packaging into exosomes remain elusive, although evidence suggests an ESCRT (Endosomal Sorting Complex Required for Transport)-independent origin to be responsible in spreading of AD pathogenesis. Intriguingly, PrP

Indexed as

Amyloid beta-PeptidesExosomesExtracellular VesiclesPrPC ProteinsAlzheimer DiseaseAnimalsEndosomal Sorting Complexes Required for TransportHumansMiceAmyloid beta-PeptidesEndosomal Sorting Complexes Required for TransportPrPC ProteinsAlzheimer’s diseaseAmyloid βESCRTExosomeExtracellular vesiclesPrion

Identifiers

PMID38970706
PMCPMC11842432

What OpenQuestion holds

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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.