Evidence map›Paper›PMID 37569510›Full record

ReviewInternational journal of molecular sciences2023

α-Synuclein Strains and Their Relevance to Parkinson's Disease, Multiple System Atrophy, and Dementia with Lewy Bodies.

Noah J Graves, Yann Gambin, Emma Sierecki

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
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  15. Article
  16. Neurodegenerative Diseases: Molecular Mechanisms and Therapies.International journal of molecular sciences · 2023
    Article
  17. Review
  18. Cannabidiol Extracted fromIranian journal of pharmaceutical research : IJPR
    Article
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

3 authors at 1 institution in 1 country.

Noah J GravesEMBL Australia Node for Single Molecule Sciences and School of Biomedical Sciences, Faculty of Medicine, The University of New South Wales, Sydney, NSW 2052, Australia.ORCID 0009-0004-5507-7838
Yann GambinEMBL Australia Node for Single Molecule Sciences and School of Biomedical Sciences, Faculty of Medicine, The University of New South Wales, Sydney, NSW 2052, Australia.
Emma SiereckiEMBL Australia Node for Single Molecule Sciences and School of Biomedical Sciences, Faculty of Medicine, The University of New South Wales, Sydney, NSW 2052, Australia.ORCID 0000-0001-9970-868X
UNSW Sydney · AU

Funding

Michael J. Fox Foundation MJFF-010267
6 · The paper itself

Abstract

Like many neurodegenerative diseases, Parkinson's disease (PD) is characterized by the formation of proteinaceous aggregates in brain cells. In PD, those proteinaceous aggregates are formed by the α-synuclein (αSyn) and are considered the trademark of this neurodegenerative disease. In addition to PD, αSyn pathological aggregation is also detected in atypical Parkinsonism, including Dementia with Lewy Bodies (DLB), Multiple System Atrophy (MSA), as well as neurodegeneration with brain iron accumulation, some cases of traumatic brain injuries, and variants of Alzheimer's disease. Collectively, these (and other) disorders are referred to as synucleinopathies, highlighting the relation between disease type and protein misfolding/aggregation. Despite these pathological relationships, however, synucleinopathies cover a wide range of pathologies, present with a multiplicity of symptoms, and arise from dysfunctions in different neuroanatomical regions and cell populations. Strikingly, αSyn deposition occurs in different types of cells, with oligodendrocytes being mainly affected in MSA, while aggregates are found in neurons in PD. If multiple factors contribute to the development of a pathology, especially in the cases of slow-developing neurodegenerative disorders, the common presence of αSyn aggregation, as both a marker and potential driver of disease, is puzzling. In this review, we will focus on comparing PD, DLB, and MSA, from symptomatology to molecular description, highlighting the role and contribution of αSyn aggregates in each disorder. We will particularly present recent evidence for the involvement of conformational strains of αSyn aggregates and discuss the reciprocal relationship between αSyn strains and the cellular milieu. Moreover, we will highlight the need for effective methodologies for the strainotyping of aggregates to ameliorate diagnosing capabilities and therapeutic treatments.

Indexed as

Lewy Body DiseaseMultiple System AtrophyParkinson DiseaseSynucleinopathiesalpha-SynucleinHumansProtein Aggregatesalpha-SynucleinProtein AggregatesSNCA protein, humanamyloid fibrilsdementia with Lewy bodiesmultiple system atrophyParkinson’s diseasestrainα-synuclein

Identifiers

PMID37569510
PMCPMC10418915
OpenAlexW4385399704

What OpenQuestion holds

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LicenceCC BY
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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.