ArticleMolecular neurodegeneration2018
Tau oligomers mediate α-synuclein toxicity and can be targeted by immunotherapy.
Article in Molecular neurodegeneration, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- Recent advances of dual PROTACs for potential therapeutic applications.Molecular diversity · 2026Review
- When Pathologies Collide: The Intersection of Tau and Alpha-Synuclein in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- From synaptic development to degeneration: a narrative review of small molecule strategies targeting alpha-synuclein in Parkinson's disease.Metabolic brain disease · 2026Review
- Amyloid-β, Tau Protein, α-Synuclein, TDP-43, and FUS in Mixed Pathology: And Intrinsic Disorder to Rule Them All.International journal of molecular sciences · 2026Review
- Targeting protein aggregate co-pathologies in neurodegeneration: a viable therapeutic strategy?Molecular neurodegeneration advances · 2026Review
- Human Wild-Type α-Synuclein Drives Progressive Tau Pathology in a Disease-Relevant Mouse Model of Synucleinopathy.Research square · 2025Article
- Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein.Molecular neurodegeneration · 2025Review
- Immunization targeting diseased proteins in synucleinopathy and tauopathy: insights from clinical trials.Translational neurodegeneration · 2025Review
- Development of Positron Emission Tomography Radiotracers for Imaging α-Synuclein Aggregates.Cells · 2025Review
- Distinct subcellular localization of tau and alpha-synuclein in lewy body disease.Acta neuropathologica communications · 2025Article
- Nigrostriatal tau pathology in parkinsonism and Parkinson's disease.Brain : a journal of neurology · 2024Article
- Tau Oligomers as Pathogenic Seeds: Preparation, Characterization, and Propagation In Vitro and In Vivo.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Protease-Sensitive and -Resistant Forms of Human and Murine Alpha-Synucleins in Distinct Brain Regions of Transgenic Mice (M83) Expressing the Human Mutated A53T Protein.Biomolecules · 2023Article
- Article
- Quercetagitrin Inhibits Tau Accumulation and Reverses Neuroinflammation and Cognitive Deficits in P301S-Tau Transgenic Mice.Molecules (Basel, Switzerland) · 2023Article
- Polymorphic Alpha-Synuclein Oligomers: Characterization and Differential Detection with Novel Corresponding Antibodies.Molecular neurobiology · 2023Article
- The Strategies of Development of New Non-Toxic Inhibitors of Amyloid Formation.International journal of molecular sciences · 2023Review
- How Well Do Rodent Models of Parkinson's Disease Recapitulate Early Non-Motor Phenotypes? A Systematic Review.Biomedicines · 2022Review
- Alpha-synuclein Immunization Strategies for Synucleinopathies in Clinical Studies: A Biological Perspective.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Synaptic Disruption by Soluble Oligomers in Patients with Alzheimer's and Parkinson's Disease.Biomedicines · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe have evaluated the efficacy of targeting the toxic, oligomeric form of tau protein by passive immunotherapy in a mouse model of synucleinopathy. Parkinson's disease and Lewy body dementia are two of the most common neurodegenerative disorders and are primarily characterized by the accumulation of α-synuclein in Lewy bodies. However, evidence shows that smaller, oligomeric aggregates are likely the most toxic form of the protein. Moreover, a large body of research suggests that α-synuclein interacts with tau in disease and may act in a synergistic mechanism, implicating tau oligomers as a potential therapeutic target.
methodsWe treated seven-month-old mice overexpressing mutated α-synuclein (A53T mice) with tau oligomer-specific monoclonal antibody (TOMA) and a control antibody and assessed both behavioral and pathological phenotypes.
resultsWe found that A53T mice treated with TOMA were protected from cognitive and motor deficits two weeks after a single injection. Levels of toxic tau oligomers were specifically decreased in the brains of TOMA-treated mice. Tau oligomer depletion also protected against dopamine and synaptic protein loss.
conclusionThese results indicate that targeting tau oligomers is beneficial for a mouse model of synucleinopathy and may be a viable therapeutic strategy for treating diseases in which tau and α-synuclein have a synergistic toxicity.
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