Evidence map›Paper›PMID 34524402›Full record

ArticleDisease models & mechanisms2021

Implications of exosomes derived from cholesterol-accumulated astrocytes in Alzheimer's disease pathology.

Qi Wu, Leonardo Cortez, Razieh Kamali-Jamil, Valerie Sim, Holger Wille, Satyabrata Kar

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

Article in Disease models & mechanisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. [Recent advances on the role of exosomes in neurodegenerative diseases].Se pu = Chinese journal of chromatography · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Cell-cell communication: new insights and clinical implications.Signal transduction and targeted therapy · 2024
    Review
  14. Review
  15. Review
  16. Article
  17. 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

6 authors at 1 institution in 1 country.

Qi WuDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB T6G 2G3, Canada.
Leonardo CortezDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB T6G 2G3, Canada.
Razieh Kamali-JamilDepartment of Biochemistry, Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB T6G 2G3, Canada.
Valerie SimDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB T6G 2G3, Canada.
Holger WilleDepartment of Biochemistry, Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB T6G 2G3, Canada.
Satyabrata KarDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB T6G 2G3, Canada.ORCID 0000-0003-0167-3808
University of Alberta · CA

Funding

CIHR
6 · The paper itself

Abstract

Amyloid β (Aβ) peptides generated from the amyloid precursor protein (APP) play a critical role in the development of Alzheimer's disease (AD) pathology. Aβ-containing neuronal exosomes, which represent a novel form of intercellular communication, have been shown to influence the function/vulnerability of neurons in AD. Unlike neurons, the significance of exosomes derived from astrocytes remains unclear. In this study, we evaluated the significance of exosomes derived from U18666A-induced cholesterol-accumulated astrocytes in the development of AD pathology. Our results show that cholesterol accumulation decreases exosome secretion, whereas lowering cholesterol increases exosome secretion, from cultured astrocytes. Interestingly, exosomes secreted from U18666A-treated astrocytes contain higher levels of APP, APP-C-terminal fragments, soluble APP, APP secretases and Aβ1-40 than exosomes secreted from control astrocytes. Furthermore, we show that exosomes derived from U18666A-treated astrocytes can lead to neurodegeneration, which is attenuated by decreasing Aβ production or by neutralizing exosomal Aβ peptide with an anti-Aβ antibody. These results, taken together, suggest that exosomes derived from cholesterol-accumulated astrocytes can play an important role in trafficking APP/Aβ peptides and influencing neuronal viability in the affected regions of the AD brain.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAndrostenesAnimalsAstrocytesAutophagyCathepsin DCells, CulturedCell SurvivalCholesterolExosomesFemaleLysosomal-Associated Membrane Protein 1LysosomesMiceMice, Inbred BALB C3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-oneAmyloid beta-PeptidesAndrostenesAnxa3 protein, ratCathepsin DCholesterolLysosomal-Associated Membrane Protein 1Microtubule-Associated ProteinsAlzheimer's diseaseAstrocytesCholesterolExosomesU18666Aβ-amyloid

Identifiers

PMID34524402
PMCPMC8560497
OpenAlexW3201083468

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.