Evidence map›Paper›PMID 29934873›Full record

ArticleActa neuropathologica2018

Alzheimer's disease pathology propagation by exosomes containing toxic amyloid-beta oligomers.

Maitrayee Sardar Sinha, Anna Ansell-Schultz, Livia Civitelli, Camilla Hildesjö, Max Larsson, Lars Lannfelt, Martin Ingelsson, Martin Hallbeck

Abstract read
In one paragraph

Article in Acta neuropathologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 323 papers.

0numbers the graph read from it
0cells of the map it votes in
323citing 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

323 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Research progress on biomarkers of traumatic brain injury.Animal models and experimental medicine · 2026
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

263 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Maitrayee Sardar SinhaDepartment of Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Anna Ansell-SchultzDepartment of Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Livia CivitelliDepartment of Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Camilla HildesjöDepartment of Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Max LarssonDepartment of Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Lars LannfeltDepartment of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden.
Martin IngelssonDepartment of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden.
Martin HallbeckDepartment of Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. Martin.Hallbeck@liu.se.ORCID 0000-0001-6716-0314

Funding

Vetenskapsrådet 523-2013-2735
6 · The paper itself

Abstract

The gradual deterioration of cognitive functions in Alzheimer's disease is paralleled by a hierarchical progression of amyloid-beta and tau brain pathology. Recent findings indicate that toxic oligomers of amyloid-beta may cause propagation of pathology in a prion-like manner, although the underlying mechanisms are incompletely understood. Here we show that small extracellular vesicles, exosomes, from Alzheimer patients' brains contain increased levels of amyloid-beta oligomers and can act as vehicles for the neuron-to-neuron transfer of such toxic species in recipient neurons in culture. Moreover, blocking the formation, secretion or uptake of exosomes was found to reduce both the spread of oligomers and the related toxicity. Taken together, our results imply that exosomes are centrally involved in Alzheimer's disease and that they could serve as targets for development of new diagnostic and therapeutic principles.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesBrainCell Line, TransformedCoculture TechniquesCulture Media, ConditionedDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportExosomesFemaleGene Expression RegulationHumansL-Lactate DehydrogenaseMaleAmyloid beta-PeptidesCulture Media, ConditionedDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportflotillinsL-Lactate DehydrogenaseMembrane ProteinsOrganic ChemicalsPeptide FragmentsPKH67Transcription FactorsTsg101 ProteinAlzheimer’s diseaseBeta-amyloidExosomesHumanOligomersPrion-likePropagation

Identifiers

PMID29934873
PMCPMC6015111

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.