Evidence map›Paper›PMID 36552674›Full record

ArticleAntioxidants (Basel, Switzerland)2022

Neuronal Oxidative Stress Promotes α-Synuclein Aggregation In Vivo.

Seok Joon Won, Rebecca Fong, Nicholas Butler, Jennifer Sanchez, Yiguan Zhang, Candance Wong, Olive Tambou Nzoutchoum, Annie Huynh, June Pan, Raymond A Swanson

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

  1. Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
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  10. Acteoside exerts neuroprotective effects by preventing α-synuclein aggregation and oxidative stress in models of Parkinson's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  11. Review
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  15. A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
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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

10 authors at 1 institution in 1 country.

Seok Joon WonDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Rebecca FongDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Nicholas ButlerDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Jennifer SanchezDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Yiguan ZhangDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Candance WongDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Olive Tambou NzoutchoumDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.ORCID 0000-0002-2344-5120
Annie HuynhDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
June PanDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Raymond A SwansonDepartment of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.ORCID 0000-0002-3664-5359
San Francisco VA Medical Center · US

Funding

Integrating pathogenic mechanisms in Parkinson's diseaseR01NS105774 · NINDS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI SWANSON, RAYMOND A · 2018 to 2022
$1.8M
BLRD VA I01 BX004884NIH HHS RO1NS105774)NINDS NIH HHS R01 NS105774
6 · The paper itself

Abstract

Both genetic and environmental factors increase risk for Parkinson's disease. Many of the known genetic factors influence α-synuclein aggregation or degradation, whereas most of the identified environmental factors produce oxidative stress. Studies using in vitro approaches have identified mechanisms by which oxidative stress can accelerate the formation of α-synuclein aggregates, but there is a paucity of evidence supporting the importance of these processes over extended time periods in brain. To assess this issue, we evaluated α-synuclein aggregates in brains of three transgenic mouse strains: hSyn mice, which overexpress human α-synuclein in neurons and spontaneously develop α-synuclein aggregates; EAAT3

Indexed as

aggregatecysteinemotor functionoxidative stressParkinson’s diseaseproximity ligation assayα-synuclein

Identifiers

PMID36552674
PMCPMC9774295
OpenAlexW4311789377

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.