Evidence map›Paper›PMID 29330884›Full record

ArticleBrain pathology (Zurich, Switzerland)2018

Synapsin III is a key component of α-synuclein fibrils in Lewy bodies of PD brains.

Francesca Longhena, Gaia Faustini, Tatiana Varanita, Michela Zaltieri, Vanessa Porrini, Isabella Tessari, Pietro Luigi Poliani, Cristina Missale, Barbara Borroni, Alessandro Padovani and 4 more

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Seeing Invisible Oligomers: Rethinking α-Synuclein Pathology Through Proximity Ligation Assay.Movement disorders : official journal of the Movement Disorder Society · 2026
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  10. Synapsin III gene silencing redeems alpha-synuclein transgenic mice from Parkinson's disease-like phenotype.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  11. Review
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  17. Differential blood DNA methylation across Lewy body dementias.Alzheimer's & dementia (Amsterdam, Netherlands) · 2021
    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

14 authors at 3 institutions in 1 country.

Francesca LonghenaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Gaia FaustiniDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Tatiana VaranitaDepartment of Biology, University of Padova, Padova, Italy.
Michela ZaltieriDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Vanessa PorriniDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Isabella TessariDepartment of Biology, University of Padova, Padova, Italy.
Pietro Luigi PolianiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Cristina MissaleDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Barbara BorroniDepartment of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.
Alessandro PadovaniDepartment of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.
Luigi BubaccoDepartment of Biology, University of Padova, Padova, Italy.
Marina PizziDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
PierFranco SpanoDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Arianna BellucciDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.ORCID 0000-0002-9581-1919
University of Brescia · ITUniversity of Padua · ITIRCCS San Camillo Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lewy bodies (LB) and Lewy neurites (LN), which are primarily composed of α-synuclein (α-syn), are neuropathological hallmarks of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). We recently found that the neuronal phosphoprotein synapsin III (syn III) controls dopamine release via cooperation with α-syn and modulates α-syn aggregation. Here, we observed that LB and LN, in the substantia nigra of PD patients and hippocampus of one subject with DLB, displayed a marked immunopositivity for syn III. The in situ proximity ligation assay revealed the accumulation of numerous proteinase K-resistant neuropathological inclusions that contained both α-syn and syn III in tight association in the brain of affected subjects. Most strikingly, syn III was identified as a component of α-syn-positive fibrils in LB-enriched protein extracts from PD brains. Finally, a positive correlation between syn III and α-syn levels was detected in the caudate putamen of PD subjects. Collectively, these findings indicate that syn III is a crucial α-syn interactant and a key component of LB fibrils in the brain of patients affected by PD.

Indexed as

AgedAged, 80 and overalpha-SynucleinAnimalsDopamineHippocampusHumansLewy BodiesMiceMice, Inbred C57BLMice, KnockoutParkinson DiseasePutamenSubstantia NigraSynapsinsalpha-SynucleinDopamineSYN3 protein, humanSynapsinsLewy bodiesLewy body dementiaParkinson's diseasesynapsin IIIα-synuclein

Identifiers

PMID29330884
PMCPMC8028549
OpenAlexW2783654252

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.