ReviewProgress in neurobiology2020
A multi-faceted genotoxic network of alpha-synuclein in the nucleus and mitochondria of dopaminergic neurons in Parkinson's disease: Emerging concepts and challenges.
Review in Progress in neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Cross-link Between CircRNAs and Neuroinflammation in Parkinson's Disease.Molecular neurobiology · 2026Review
- The vicious cycle: unraveling the interplay between α-synuclein, mitochondrial dysfunction, and neuroinflammation in Parkinson's disease.Journal of neurology · 2026Review
- Calcium overload induced mitochondrial and lysosomal dysfunction is regulated by Tousled-like kinase in a-synucleinopathy.Cell death & disease · 2026Article
- Role of mitochondria in physiological activities, diseases, and therapy.Molecular biomedicine · 2025Review
- Exploring the Role of Ubiquitin-Proteasome System in the Pathogenesis of Parkinson's Disease.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Review
- Relationship among α‑synuclein, aging and inflammation in Parkinson's disease (Review).Experimental and therapeutic medicine · 2024Review
- α-Synuclein Promotes Neuronal Dysfunction and Death by Disrupting the Binding of Ankyrin to β-Spectrin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- α-Synuclein and Mechanisms of Epigenetic Regulation.Brain sciences · 2023Review
- 1. Parkinson's disease - Perspectives from Alpha-synuclein related pathogenesis and current research.Journal of stem cells & regenerative medicine · 2023Article
- Complex modulation of cytokine-induced α-synuclein aggregation by glypican-1-derived heparan sulfate in neural cells.Glycobiology · 2022Article
- Rosmarinic Acid Inhibits Mitochondrial Damage by Alleviating Unfolded Protein Response.Frontiers in pharmacology · 2022Article
- Molecular insights into α-synuclein interaction with individual human core histones, linker histone, and dsDNA.Protein science : a publication of the Protein Society · 2021Article
- Oral Administration of Silibinin Ameliorates Cognitive Deficits of Parkinson's Disease Mouse Model by Restoring Mitochondrial Disorders in Hippocampus.Neurochemical research · 2021Article
- Article
- Roles for α-Synuclein in Gene Expression.Genes · 2021Review
- α-Synuclein A53T Binds to Transcriptional Adapter 2-Alpha and Blocks Histone H3 Acetylation.International journal of molecular sciences · 2021Article
- Mechanisms of Neurodegeneration in Various Forms of Parkinsonism-Similarities and Differences.Cells · 2021Review
- Remodeling of the Conformational Dynamics of Noncanonical DNA Structures by Monomeric and Aggregated α-Synuclein.Journal of the American Chemical Society · 2020Article
- Ethionine Suppresses Mitochondria Autophagy and Induces Apoptosis via Activation of Reactive Oxygen Species in Neural Tube Defects.Frontiers in neurology · 2020Article
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Authors and funding
6 authors.
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Abstract
α-Synuclein is a hallmark amyloidogenic protein component of the Lewy bodies (LBs) present in dopaminergic neurons affected by Parkinson's disease (PD). Despite an enormous increase in emerging knowledge, the mechanism(s) of α-synuclein neurobiology and crosstalk among pathological events that are critical for PD progression remains enigmatic, creating a roadblock for effective intervention strategies. One confounding question is about the potential link between α-synuclein toxicity and genome instability in PD. We previously reported that pro-oxidant metal ions, together with reactive oxygen species (ROS), act as a "double whammy" in dopaminergic neurons by not only inducing genome damage but also inhibiting their repair. Our recent studies identified a direct role for chromatin-bound, oxidized α-synuclein in the induction of DNA strand breaks, which raised the question of a paradoxical role for α-synuclein's DNA binding in neuroprotection versus neurotoxicity. Furthermore, recent advances in our understanding of α-synuclein mediated mitochondrial dysfunction warrants revisiting the topics of α-synuclein pathophysiology in order to devise and assess the efficacy of α-synuclein-targeted interventions. In this review article, we discuss the multi-faceted neurotoxic role of α-synuclein in the nucleus and mitochondria with a particular emphasis on the role of α-synuclein in DNA damage/repair defects. We utilized a protein-DNA binding simulation to identify potential residues in α-synuclein that could mediate its binding to DNA and may be critical for its genotoxic functions. These emerging insights and paradigms may guide new drug targets and therapeutic modalities.
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