ArticleHuman molecular genetics2014
Interactions between Tau and α-synuclein augment neurotoxicity in a Drosophila model of Parkinson's disease.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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50 citing papers in PubMed, 72 citations in OpenAlex.
- Polyamine metabolic enzyme SAT1 remodels the neuronal transcriptome and rescues α-synuclein toxicity in Drosophila.Amino acids · 2026Article
- Tau physiology and pathology: impacts on cellular structures and neurodegenerative diseases.Inflammopharmacology · 2026Review
- Histone modification dynamics in brain aging: unlocking therapeutic potential.Cell death & disease · 2026Review
- Immune crosstalk in Alzheimer's and Parkinson's disease: insights from Drosophila models into the brain-peripheral immune axis.Frontiers in immunology · 2026Review
- Exploring the versatility ofFly · 2025Review
- Disease-disease interactions: molecular links of neurodegenerative diseases with cancer, viral infections, and type 2 diabetes.Translational neurodegeneration · 2025Review
- Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein.Molecular neurodegeneration · 2025Review
- Co-Aggregation of TDP-43 with Other Pathogenic Proteins and Their Co-Pathologies in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Genetic forms of tauopathies: inherited causes and implications of Alzheimer's disease-like TAU pathology in primary and secondary tauopathies.Journal of neurology · 2024Review
- Overlaps and divergences between tauopathies and synucleinopathies: a duet of neurodegeneration.Translational neurodegeneration · 2024Review
- Advancements in Genetic and Biochemical Insights: Unraveling the Etiopathogenesis of Neurodegeneration in Parkinson's Disease.Biomolecules · 2024Review
- Common mechanisms underlying axonal transport deficits in neurodegenerative diseases: a mini review.Frontiers in molecular neuroscience · 2023Review
- Molecular mechanism for the synchronized electrostatic coacervation and co-aggregation of alpha-synuclein and tau.Nature communications · 2022Article
- Drug discovery from natural products - Old problems and novel solutions for the treatment of neurodegenerative diseases.Journal of pharmaceutical and biomedical analysis · 2022Review
- Roles of α-Synuclein and Disease-Associated Factors inInternational journal of molecular sciences · 2022Review
- Exploring therapeutic potential of mitophagy modulators usingFrontiers in aging neuroscience · 2022Review
- Potential value of cerebrospinal fluid α-synuclein in the identification of postoperative delirium undergoing knee/hip arthroplasty: The perioperative neurocognitive disorder and biomarker lifestyle study.Frontiers in neuroscience · 2022Article
- Chronic Exposure to Paraquat Induces Alpha-Synuclein Pathogenic Modifications inInternational journal of molecular sciences · 2021Article
- Interplay between tau and α-synuclein liquid-liquid phase separation.Protein science : a publication of the Protein Society · 2021Article
- The cell biology of Parkinson's disease.The Journal of cell biology · 2021Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
Clinical and pathological studies have suggested considerable overlap between tauopathies and synucleinopathies. Several genome-wide association studies have identified alpha-Synuclein (SNCA) and Tau (MAPT) polymorphisms as common risk factors for sporadic Parkinson's disease (PD). However, the mechanisms by which subtle variations in the expression of wild-type SNCA and MAPT influence risk for PD and the underlying cellular events that effect neurotoxicity remain unclear. To examine causes of neurotoxicity associated with the α-Syn/Tau interaction, we used the fruit fly as a model. We utilized misexpression paradigms in three different tissues to probe the α-Syn/Tau interaction: the retina, dopaminergic neurons and the larval neuromuscular junction. Misexpression of Tau and α-Syn enhanced a rough eye phenotype and loss of dopaminergic neurons in fly tauopathy and synucleinopathy models, respectively. Our findings suggest that interactions between α-Syn and Tau at the cellular level cause disruption of cytoskeletal organization, axonal transport defects and aberrant synaptic organization that contribute to neuronal dysfunction and death associated with sporadic PD. α-Syn did not alter levels of Tau phosphorylated at the AT8 epitope. However, α-Syn and Tau colocalized in ubiquitin-positive aggregates in eye imaginal discs. The presence of Tau also led to an increase in urea soluble α-Syn. Our findings have important implications in understanding the cellular and molecular mechanisms underlying α-Syn/Tau-mediated synaptic dysfunction, which likely arise in the early asymptomatic phase of sporadic PD.
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