Evidence mapPaperPMID 39212313Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024

Cellular prion protein acts as mediator of amyloid beta uptake by caveolin-1 causing cellular dysfunctions in vitro and in vivo.

Angela da Silva Correia, Matthias Schmitz, Anna-Lisa Fischer, Susana da Silva Correia, Franco L Simonetti, Gesine Saher, Roberto Goya-Maldonado, Amandeep Singh Arora, Andre Fischer, Tiago F Outeiro and 1 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. The PDE5 inhibitor vardenafil enhances glutamatergic transmission through amyloid-beta and cellular prion protein.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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

11 authors.

Angela da Silva CorreiaDepartment of Neurology, University Medical Center and the German Center for Neurodegenerative Diseases (DZNE), Georg-August University, Goettingen, Germany.
Matthias SchmitzDepartment of Neurology, University Medical Center and the German Center for Neurodegenerative Diseases (DZNE), Georg-August University, Goettingen, Germany.
Anna-Lisa FischerDepartment of Neurology, University Medical Center and the German Center for Neurodegenerative Diseases (DZNE), Georg-August University, Goettingen, Germany.
Susana da Silva CorreiaDepartment of Neurology, University Medical Center and the German Center for Neurodegenerative Diseases (DZNE), Georg-August University, Goettingen, Germany.
Franco L SimonettiFundación Instituto Leloir, Buenos Aires, Argentina.
Gesine SaherDepartment of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Goettingen, Germany.
Roberto Goya-MaldonadoLaboratory of Systems Neuroscience and Imaging in Psychiatry (SNIP-Lab), Department of Psychiatry and Psychotherapy, University Medical Center Goettingen (UMG), Goettingen, Germany.
Amandeep Singh AroraTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Andre FischerDepartment of Psychiatry and Psychotherapy, University Medical Center Goettingen, Goettingen, Germany.
Tiago F OuteiroDepartment of Experimental Neurodegeneration, Center for Nanoscale Microscopy and Molecular Physiology of the Brain, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Goettingen, Goettingen, Germany.
Inga ZerrDepartment of Neurology, University Medical Center and the German Center for Neurodegenerative Diseases (DZNE), Georg-August University, Goettingen, Germany.

Funding

Alzheimer Forschung Initiative 12851Alzheimer Forschung Initiative 20026
6 · The paper itself

Abstract

introductionCellular prion protein (PrP

methodsDouble transgenic mice were generated by crossing Prnp knockout (KO) with 5xFAD mice, and light-sheet microscopy was used for whole brain tissue analyses. PrP

resultsIn vivo, PrP DISCUSSION: The findings shed new light on the relevance of intracellular Aβo, suggesting that PrP HIGHLIGHTS: PrP

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCaveolin 1Prion ProteinsAnimalsBrainDisease Models, AnimalHumansMiceMice, KnockoutMice, TransgenicNeuronsPlaque, AmyloidPrPC ProteinsAmyloid beta-PeptidesCaveolin 1Prion ProteinsPrnp protein, mousePrPC ProteinsAlzheimer's diseaseamyloid betacaveolincellular prion protein

Identifiers

PMID39212313
PMCPMC11485400

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.