Evidence map›Paper›PMID 39704040›Full record

ReviewMedicinal research reviews2025

α-Synuclein in Parkinson's Disease: From Bench to Bedside.

Gabriele Bellini, Vanessa D'Antongiovanni, Giovanni Palermo, Luca Antonioli, Matteo Fornai, Roberto Ceravolo, Nunzia Bernardini, Pascal Derkinderen, Carolina Pellegrini

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Medicinal research reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  6. Molecularly Engineered Phenoxazinone-Skeleton Cascade-Activated NIR Probes for Monitoring FeAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Neuroprotective Effects ofPharmaceuticals (Basel, Switzerland) · 2026
    Article
  8. Article
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  11. 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

9 authors.

Gabriele BelliniCenter for Neurodegenerative Diseases, Unit of Neurology, Parkinson's Disease and Movement Disorders, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.ORCID 0000-0002-0648-6836
Vanessa D'AntongiovanniUnit of Histology and Embryology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.ORCID 0000-0002-3303-0674
Giovanni PalermoCenter for Neurodegenerative Diseases, Unit of Neurology, Parkinson's Disease and Movement Disorders, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Luca AntonioliUnit of Pharmacology and Pharmacovigilance, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Matteo FornaiUnit of Pharmacology and Pharmacovigilance, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Roberto CeravoloCenter for Neurodegenerative Diseases, Unit of Neurology, Parkinson's Disease and Movement Disorders, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Nunzia BernardiniUnit of Histology and Embryology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Pascal DerkinderenDepartment of Neurology, Nantes Université, CHU Nantes, INSERM, Nantes, France.
Carolina PellegriniUnit of Histology and Embryology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.ORCID 0000-0003-2644-5430

Funding

The authors received no specific funding for this work.
6 · The paper itself

Abstract

α-Synuclein (α-syn), a pathological hallmark of PD, is emerging as a bridging element at the crossroads between neuro/immune-inflammatory responses and neurodegeneration in PD. Several evidence show that pathological α-syn accumulates in neuronal and non-neuronal cells (i.e., neurons, microglia, macrophages, skin cells, and intestinal cells) in central and peripheral tissues since the prodromal phase of the disease, contributing to brain pathology. Indeed, pathological α-syn deposition can promote neurogenic/immune-inflammatory responses that contribute to systemic and central neuroinflammation associated with PD. After providing an overview of the structure and functions of physiological α-syn as well as its pathological forms, we review current studies about the role of neuronal and non-neuronal α-syn at the crossroads between neuroinflammation and neurodegeneration in PD. In addition, we provide an overview of the correlation between the accumulation of α-syn in central and peripheral tissues and PD, related symptoms, and neuroinflammation. Special attention was paid to discussing whether targeting α-syn can represent a suitable therapeutical approach for PD.

Indexed as

alpha-SynucleinParkinson DiseaseTranslational Research, BiomedicalAnimalsHumansInflammationNeuronsalpha-Synucleincentral nervous systemclinical trialsgut‐brain axisimmune cellsneurodegenerationneuroinflammationParkinson's diseasepreclinical evidencespreadingα‐synuclein

Identifiers

PMID39704040
PMCPMC11976381

What OpenQuestion holds

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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.