ArticleInternational journal of molecular sciences2020
The Down-Regulation of Clusterin Expression Enhances the αSynuclein Aggregation Process.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- The quest for Parkinson's disease biomarkers: traditional and emerging multi-omics approaches.Molecular biology reports · 2025Review
- The Emerging Role of the Molecular Chaperone Clusterin in Parkinson's Disease.International journal of molecular sciences · 2025Review
- Connexin 43 is downregulated in advanced Parkinson's disease in multiple brain regions which correlates with symptoms.Scientific reports · 2025Article
- Discovery of a small molecule secreted clusterin enhancer that improves memory in Alzheimer's disease mice.npj drug discovery · 2025Article
- Article
- Can exercise benefits be harnessed with drugs? A new way to combat neurodegenerative diseases by boosting neurogenesis.Translational neurodegeneration · 2024Review
- Clusterin is a Potential Therapeutic Target in Alzheimer's Disease.Molecular neurobiology · 2024Review
- Clusterin: a double-edged sword in cancer and neurological disorders.EXCLI journal · 2024Review
- Protein Biomarkers Shared by Multiple Neurodegenerative Diseases Are Calmodulin-Binding Proteins Offering Novel and Potentially Universal Therapeutic Targets.Journal of clinical medicine · 2023Review
- Uncovering the Role of Natural and Synthetic Small Molecules in Counteracting the Burden of α-Synuclein Aggregates and Related Toxicity in Different Models of Parkinson's Disease.International journal of molecular sciences · 2023Review
- Recent advances on the molecular mechanisms of exercise-induced improvements of cognitive dysfunction.Translational neurodegeneration · 2023Review
- Unexpected Absence of Skeletal Responses to Dietary Magnesium Depletion: Basis for Future Perspectives?Biomedicines · 2023Article
- Magnetic transferrin nanoparticles (MTNs) assay as a novel isolation approach for exosomal biomarkers in neurological diseases.Biomaterials research · 2023Article
- Closest horizons of Hsp70 engagement to manage neurodegeneration.Frontiers in molecular neuroscience · 2023Review
- Transcriptomes of Clusterin- and S100B-transfected neuronal cells elucidate protective mechanisms against hypoxia and oxidative stress in the hooded seal (Cystophora cristata) brain.BMC neuroscience · 2022Article
- HDL Accessory Proteins in Parkinson's Disease-Focusing on Clusterin (Apolipoprotein J) in Regard to Its Involvement in Pathology and Diagnostics-A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Calmodulin binding proteins and neuroinflammation in multiple neurodegenerative diseases.BMC neuroscience · 2022Review
- Inhibition of Neuroinflammation May Mediate the Disease-Modifying Effects of Exercise: Implications for Parkinson's Disease.Journal of Parkinson's disease · 2022Article
- Cell Signaling in Neurodegeneration.International journal of molecular sciences · 2021Article
- The extracellular chaperone Clusterin enhances Tau aggregate seeding in a cellular model.Nature communications · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's Disease (PD) is a progressive neurodegenerative disease characterized by the presence of proteinaceous aggregates of αSynuclein (αSyn) in the dopaminergic neurons. Chaperones are key components of the proteostasis network that are able to counteract αSyn's aggregation, as well as its toxic effects. Clusterin (CLU), a molecular chaperone, was consistently found to interfere with Aβ aggregation in Alzheimer's Disease (AD). However, its role in PD pathogenesis has yet to be extensively investigated. In this study, we assessed the involvement of CLU in the αSyn aggregation process by using SH-SY5Y cells stably overexpressing αSyn (SH-Syn). First, we showed that αSyn overexpression caused a strong increase in CLU expression without affecting levels of Hsp27, Hsp70, and Hsp90, which are the chaperones widely recognized to counteract αSyn burden. Then, we demonstrated that αSyn aggregation, induced by proteasome inhibition, determines a strong increase of CLU in insoluble aggregates. Remarkably, we revealed that CLU down-regulation results in an increase of αSyn aggregates in SH-Syn without significantly affecting cell viability and the Unfolded Protein Response (UPR). Furthermore, we demonstrated the direct molecular interaction between CLU and αSyn via a co-immunoprecipitation (co-IP) assay. All together, these findings provide incontrovertible evidence that CLU is an important player in the response orchestrated by the cell to cope with αSyn burden.
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