ArticleJournal of molecular neuroscience : MN2009
Parkin attenuates wild-type tau modification in the presence of beta-amyloid and alpha-synuclein.
Article in Journal of molecular neuroscience : MN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
What it found
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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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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.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- E3 ubiquitin ligases in neurodegenerative diseases.Military Medical Research · 2026Review
- Parkin as a Molecular Bridge Linking Alzheimer's and Parkinson's Diseases?Biomolecules · 2022Review
- Interaction between Parkin andCells · 2021Review
- Review
- Is human immunodeficiency virus-mediated dementia an autophagic defect that leads to neurodegeneration?CNS & neurological disorders drug targets · 2014Review
- PESCADOR, a web-based tool to assist text-mining of biointeractions extracted from PubMed queries.BMC bioinformatics · 2011Article
- Beta-amyloid1-42 gene transfer model exhibits intraneuronal amyloid, gliosis, tau phosphorylation, and neuronal loss.The Journal of biological chemistry · 2010Article
- The Relationship between Parkin and Protein Aggregation in Neurodegenerative Diseases.Frontiers in psychiatry · 2010Article
- Parkin promotes intracellular Abeta1-42 clearance.Human molecular genetics · 2009Article
Corrections and comments
- Erratum issued
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Changes in tau (tau) metabolism comprise important pathological landmarks in the tauopathies with parkinsonism as well as Parkinson's disease and Alzheimer's disease. Mutations in the parkin gene are associated with Parkinson's disease. Deposits of amyloid proteins, including Abeta and alpha-synuclein coexist in the brains of patients with dementia with Lewy bodies; however, it is not known how either of them interacts with tau to provoke neurofibrillary tangle formation across the tauopathies. Here, we show a role for parkin against tau pathology in the presence of intracellular Abeta or alpha-synuclein. Parkin attenuates four-repeat human tau, but not mutant P301L, hyperphosphorylation in the presence of intracellular Abeta(1-42), or alpha-synuclein and decreases GSK-3beta activity in amyloid-stressed M17 human neuroblastoma cells. These data suggest that parkin may counteract the alteration of tau metabolism in certain neurodegenerative diseases with tau cytopathy and parkinsonism.
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Registered trials
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