Evidence map›Paper›PMID 36399706›Full record

ArticlePloS one2022

Human pericytes degrade diverse α-synuclein aggregates.

Birger Victor Dieriks, Blake Highet, Ania Alik, Tracy Bellande, Taylor J Stevenson, Victoria Low, Thomas I-H Park, Jason Correia, Patrick Schweder, Richard L M Faull and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Pericytes in the optic nerve head.Progress in retinal and eye research · 2025
    Review
  10. Article
  11. Review
  12. Article
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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

13 authors at 1 institution in 1 country.

Birger Victor DieriksDepartment of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.ORCID 0000-0002-9392-3327
Blake HighetDepartment of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.
Ania AlikMolecular Imaging Research Center, Francois Jacob Institute, Alternative Energies and Atomic Energy Commission, and Laboratory of Neurodegenerative Diseases, National Center for Scientific Research, Fontenay- Aux-Roses, France.
Tracy BellandeMolecular Imaging Research Center, Francois Jacob Institute, Alternative Energies and Atomic Energy Commission, and Laboratory of Neurodegenerative Diseases, National Center for Scientific Research, Fontenay- Aux-Roses, France.
Taylor J StevensonDepartment of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.ORCID 0000-0001-6032-1445
Victoria LowDepartment of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.
Thomas I-H ParkCentre for Brain Research, University of Auckland, Auckland, New Zealand.
Jason CorreiaCentre for Brain Research, University of Auckland, Auckland, New Zealand.
Patrick SchwederCentre for Brain Research, University of Auckland, Auckland, New Zealand.
Richard L M FaullDepartment of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.
Ronald MelkiMolecular Imaging Research Center, Francois Jacob Institute, Alternative Energies and Atomic Energy Commission, and Laboratory of Neurodegenerative Diseases, National Center for Scientific Research, Fontenay- Aux-Roses, France.
Maurice A CurtisDepartment of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.
Mike DragunowCentre for Brain Research, University of Auckland, Auckland, New Zealand.
University of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive, neurodegenerative disorder characterised by the abnormal accumulation of α-synuclein (α-syn) aggregates. Central to disease progression is the gradual spread of pathological α-syn. α-syn aggregation is closely linked to progressive neuron loss. As such, clearance of α-syn aggregates may slow the progression of PD and lead to less severe symptoms. Evidence is increasing that non-neuronal cells play a role in PD and other synucleinopathies such as Lewy body dementia and multiple system atrophy. Our previous work has shown that pericytes-vascular mural cells that regulate the blood-brain barrier-contain α-syn aggregates in human PD brains. Here, we demonstrate that pericytes efficiently internalise fibrillar α-syn irrespective of being in a monoculture or mixed neuronal cell culture. Pericytes cleave fibrillar α-syn aggregates (Fibrils, Ribbons, fibrils65, fibrils91 and fibrils110), with cleaved α-syn remaining present for up to 21 days. The number of α-syn aggregates/cell and average aggregate size depends on the type of strain, but differences disappear within 5 five hours of treatment. Our results highlight the role brain vasculature may play in reducing α-syn aggregate burden in PD.

Indexed as

Lewy Body DiseaseParkinson Diseasealpha-SynucleinHumansNeuronsPericytesalpha-Synuclein

Identifiers

PMID36399706
PMCPMC9674377
OpenAlexW4309353194

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.