Evidence map›Paper›PMID 26780457›Full record

ArticleMolecular neurobiology2017

Perforin Promotes Amyloid Beta Internalisation in Neurons.

Erica Lana, Mahbod Khanbolouki, Charline Degavre, Eva-Britt Samuelsson, Elisabet Åkesson, Bengt Winblad, Evren Alici, Christina Unger Lithner, Homira Behbahani

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Antigen-specific age-related memory CD8 T cells induce and track Alzheimer's-like neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  15. Pioglitazone Reduces β Amyloid LevelsFrontiers in aging neuroscience · 2019
    Article
  16. 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

9 authors at 2 institutions in 1 country.

Erica LanaDivision of Translational Alzheimer Neurobiology, NVS Department, Center for Alzheimer Research, Karolinska Institutet, Huddinge, 141 57, Sweden.
Mahbod KhanboloukiDivision for Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Center for Alzheimer Research, Karolinska Institutet, Novum 5th floor, Huddinge, 141 57, Sweden.
Charline DegavreDivision for Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Center for Alzheimer Research, Karolinska Institutet, Novum 5th floor, Huddinge, 141 57, Sweden.
Eva-Britt SamuelssonDivision of Neurodegeneration, NVS Department, Center for Alzheimer Research, Karolinska Institutet, Huddinge, 141 57, Sweden.
Elisabet ÅkessonDivision of Neurodegeneration, NVS Department, Center for Alzheimer Research, Karolinska Institutet, Huddinge, 141 57, Sweden.
Bengt WinbladDivision for Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Center for Alzheimer Research, Karolinska Institutet, Novum 5th floor, Huddinge, 141 57, Sweden.
Evren AliciDivision of Hematology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Huddinge, 141 57, Sweden.
Christina Unger LithnerDivision of Translational Alzheimer Neurobiology, NVS Department, Center for Alzheimer Research, Karolinska Institutet, Huddinge, 141 57, Sweden.
Homira BehbahaniDivision for Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Center for Alzheimer Research, Karolinska Institutet, Novum 5th floor, Huddinge, 141 57, Sweden. homira.behbahani@ki.se.ORCID 0000-0002-2612-0858
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies on the mechanisms of neuronal amyloid-β (Aβ) internalisation are crucial for understanding the neuropathological progression of Alzheimer's disease (AD). We here investigated how extracellular Aβ peptides are internalised and focused on three different pathways: (i) via endocytic mechanisms, (ii) via the receptor for advanced glycation end products (RAGE) and (iii) via the pore-forming protein perforin. Both Aβ

Indexed as

Amyloid beta-PeptidesCell Line, TumorCells, CulturedCerebral CortexEndocytosisHumansNeuronsPeptide FragmentsPerforinAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Peptide FragmentsPerforinAlzheimer’s diseaseAmyloid β peptidesEndocytosisHuman primary neuronsPerforinRAGESH-SY5Y

Identifiers

PMID26780457
OpenAlexW2301395465

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.