ReviewInternational journal of molecular sciences2012
Possible alterations in β-Synuclein, the non-amyloidogenic homologue of α-Synuclein, during progression of sporadic α-synucleinopathies.
Review in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Comparative Analysis of Aggregation of β- and γ-Synucleins in Vertebrates.Biomolecules · 2025Article
- Therapeutic Potential ofParkinson's disease · 2021Review
- Hydrogen Sulfide andJournal of ophthalmology · 2020Article
- Interactions between the Intrinsically Disordered Proteins β-Synuclein and α-Synuclein.Proteomics · 2018Review
- Diversity of mitochondrial pathology in a mouse model of axonal degeneration in synucleinopathies.Oxidative medicine and cellular longevity · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
α-Synucleinopathies are neurodegenerative disorders that are characterized by progressive decline of motor and non-motor dysfunctions. α-Synuclein (αS) has been shown to play a causative role in neurodegeneration, but the pathogenic mechanisms are still unclear. Thus, there are no radical therapies that can halt or reverse the disease's progression. β-Synuclein (βS), the non-amyloidogenic homologue of αS, ameliorates the neurodegeneration phenotype of αS in transgenic (tg) mouse models, as well as in cell free and cell culture systems, which suggests that βS might be a negative regulator of neurodegeneration caused by αS, and that "loss of function" of βS might be involved in progression of α-synucleinopathies. Alternatively, it is possible that "toxic gain of function" of wild type βS occurs during the pathogenesis of sporadic α-synucleinopathies, since tg mice expressing dementia with Lewy bodies-linked P123H βS develop progressive neurodegeneration phenotypes, such as axonal pathology and dementia. In this short review, we emphasize the aspects of "toxic gain of function" of wild type βS during the pathogenesis of sporadic α-synucleinopathies.
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Registered trials
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