ArticleJournal of neuroinflammation2020
Phagocytosis of full-length Tau oligomers by Actin-remodeling of activated microglia.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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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Who cites it
44 citing papers in PubMed, 115 citations in OpenAlex.
- Rethinking tau-targeted therapy in Alzheimer's disease: Toward a dual biomarker strategy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Hippocampal neural stem cell-derived extracellular vesicles modulate microglia to promote resilience against tau oligomers.Neural regeneration research · 2026Article
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Meningeal macrophages alleviate social memory defects in an early Alzheimer's disease model.Molecular psychiatry · 2026Article
- The spleen-brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Tau abnormalities and microglial remodeling in glaucoma: potential links to phagocytosis-related injury.Frontiers in neurology · 2026Review
- Glial phagocytosis for synapse and toxic proteins in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- The transcriptional and cellular landscape of cognitive resilience to Alzheimer's disease.Frontiers in molecular neuroscience · 2025Review
- CX3CR1: a potential microglia-specific PET imaging target in Alzheimer's and Parkinson's diseases.Frontiers in pharmacology · 2025Review
- Cerebral hypoperfusion reduces tau accumulation.Annals of clinical and translational neurology · 2025Article
- Modulation of Oxidative Stress and Neuroinflammation by Cannabidiol (CBD): Promising Targets for the Treatment of Alzheimer's Disease.Current issues in molecular biology · 2024Review
- The Enigma of Tau Protein Aggregation: Mechanistic Insights and Future Challenges.International journal of molecular sciences · 2024Review
- Experience-dependent glial pruning of synaptic glomeruli during the critical period.Scientific reports · 2024Article
- Clathrin mediated endocytosis in Alzheimer's disease: cell type specific involvement in amyloid beta pathology.Frontiers in aging neuroscience · 2024Review
- Tau deficiency inhibits classically activated macrophage polarization and protects against collagen-induced arthritis in mice.Arthritis research & therapy · 2023Article
- Extracellular tau stimulates phagocytosis of living neurons by activated microglia via Toll-like 4 receptor-NLRP3 inflammasome-caspase-1 signalling axis.Scientific reports · 2023Article
- Friend or foe: role of pathological tau in neuronal death.Molecular psychiatry · 2023Review
- Microglia degrade Tau oligomers deposit via purinergic P2Y12-associated podosome and filopodia formation and induce chemotaxis.Cell & bioscience · 2023Article
- Review
- Actin-dependent astrocytic infiltration is a key step for axon defasciculation during remodeling.Cell reports · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlzheimer's disease is associated with the accumulation of intracellular Tau tangles within neurons and extracellular amyloid-β plaques in the brain parenchyma, which altogether results in synaptic loss and neurodegeneration. Extracellular concentrations of oligomers and aggregated proteins initiate microglial activation and convert their state of synaptic surveillance into a destructive inflammatory state. Although Tau oligomers have fleeting nature, they were shown to mediate neurotoxicity and microglial pro-inflammation. Due to the instability of oligomers, in vitro experiments become challenging, and hence, the stability of the full-length Tau oligomers is a major concern.
methodsIn this study, we have prepared and stabilized hTau40
resultsFull-length Tau oligomers were detected in heterogeneous globular structures ranging from 5 to 50 nm as observed by high-resolution transmission electron microscopy, which was further characterized by oligomer-specific A11 antibody. Immunocytochemistry studies for oligomer treatment were evidenced with A11
conclusionThe peri-membrane polymerization of actin filament and co-localization of Iba1 relate to the microglial movements for phagocytosis. Here, these findings suggest that microglia modified actin cytoskeleton for phagocytosis and rapid clearance of Tau oligomers in Alzheimer's disease condition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.