ArticleMolecular and cellular biochemistry2018
Alpha-synuclein aggregation, Ubiquitin proteasome system impairment, and L-Dopa response in zinc-induced Parkinsonism: resemblance to sporadic Parkinson's disease.
Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Postnatal Exposure Sensitizes for Zinc/Paraquat-Induced Neuronal Apoptosis, Adulthood Exposure Leads to the Final Effects.Journal of molecular neuroscience : MN · 2026Article
- Metallothionein and neurodegenerative diseases.Neural regeneration research · 2026Article
- Parkinson's Disease: The Epidemiology, Risk Factors, Molecular Pathogenesis, Prevention, and Therapy.MedComm · 2025Review
- An update on the involvement of inflammatory mediators in Parkinson's disease pathogenesis.Archives of toxicology · 2025Review
- Zinc-Dependent Modulation of Dopamine Release and Uptake Is Altered in Parkinson's Disease Model Zebrafish.ACS chemical neuroscience · 2025Article
- Impaired Mitochondrial Function and Ubiquitin Proteasome System Activate α-Synuclein Aggregation in Zinc-Induced Neurotoxicity: Effect of Antioxidants.Journal of molecular neuroscience : MN · 2025Article
- Alpha-synuclein modulates the repair of genomic DNA double-strand breaks in a DNA-PKNeurobiology of disease · 2024Article
- Unraveling the mechanistic interplay of mediators orchestrating the neuroprotective potential of harmine.Pharmacological reports : PR · 2024Review
- Tetramethylpyrazine Nitrone Promotes the Clearance of Alpha-Synuclein via Nrf2-Mediated Ubiquitin-Proteasome System Activation.Neuromolecular medicine · 2024Article
- Autophagy and UPS pathway contribute to nicotine-induced protection effect in Parkinson's disease.Experimental brain research · 2024Article
- Heavy Metal Mediated Progressive Degeneration and Its Noxious Effects on Brain Microenvironment.Biological trace element research · 2024Review
- Emerging role of microglia in inter-cellular transmission of α-synuclein in Parkinson's disease.Frontiers in aging neuroscience · 2024Review
- Proteasome localization and activity in pig brain andFrontiers in cellular neuroscience · 2024Article
- Is alumina suitable for solid phase extraction of catecholamines from brain tissue?Arhiv za higijenu rada i toksikologiju · 2023Article
- Zinc Homeostasis: An Emerging Therapeutic Target for Neuroinflammation Related Diseases.Biomolecules · 2023Review
- The Zinc Ionophore Clioquinol Reduces Parkinson's Disease Patient-Derived Brain Extracts-Induced Neurodegeneration.Molecular neurobiology · 2022Article
- ATP13A2 Declines Zinc-Induced Accumulation of α-Synuclein in a Parkinson's Disease Model.International journal of molecular sciences · 2022Article
- p21-activated kinase 4 controls the aggregation of α-synuclein by reducing the monomeric and aggregated forms of α-synuclein: involvement of the E3 ubiquitin ligase NEDD4-1.Cell death & disease · 2022Article
- Mitochondrial Dysfunction Contributes To Zinc-induced Neurodegeneration: a Link with NADPH Oxidase.Journal of molecular neuroscience : MN · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Alpha-synuclein (α-synuclein) aggregation and impairment of the Ubiquitin proteasome system (UPS) are implicated in Parkinson's disease (PD) pathogenesis. While zinc (Zn) induces dopaminergic neurodegeneration resulting in PD phenotype, its effect on protein aggregation and UPS has not yet been deciphered. The current study investigated the role of α-synuclein aggregation and UPS in Zn-induced Parkinsonism. Additionally, levodopa (L-Dopa) response was assessed in Zn-induced Parkinsonian model to establish its closeness with idiopathic PD. Male Wistar rats were treated with zinc sulfate (Zn; 20 mg/kg; i.p.) twice weekly for 12 weeks along with respective controls. In few subsets, animals were subsequently treated with L-Dopa for 21 consecutive days following Zn exposure. A significant increase in total and free Zn content was observed in the substantia nigra of the brain of exposed groups. Zn treatment caused neurobehavioral anomalies, striatal dopamine decline, and dopaminergic neuronal cell loss accompanied with a marked increase in α-synuclein expression/aggregation and Ubiquitin-conjugated protein levels in the exposed groups. Zn exposure substantially reduced UPS-associated trypsin-like, chymotrypsin-like, and caspase-like activities along with the expression of SUG1 and β-5 subunits of UPS in the nigrostriatal tissues of exposed groups. L-Dopa treatment rescued from Zn-induced neurobehavioral deficits and restored dopamine levels towards normalcy; however, Zn-induced dopaminergic neuronal loss, reduction in tyrosine hydroxylase expression, and increase in oxidative stress were unaffected. The results suggest that Zn caused UPS impairment, resulting in α-synuclein aggregation subsequently leading to dopaminergic neurodegeneration, and that Zn-induced Parkinsonism exhibited positive L-Dopa response similar to sporadic PD.
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