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30 results

Hypothesis Inhibiting Heparan Sulfate Proteoglycan Receptor-Mediated Neuronal Tau Uptake rel 7.00

tau pathology, including tau immunotherapy, microtubule-stabilizing agents, and tau

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Hypothesis Excitatory Neuron Synaptic Dysfunction and Mitochondrial Stress via MAPT (tau) rel 6.00

tau's toxic effects on cellular energetics. Tau pathology disrupts

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Hypothesis Conformational-Selective Blocking of Tau Uptake Reveals Therapeutic Window in Neuronal Re-entry rel 5.00

tau pathology. The conformational selectivity arises from pathological tau's adoption

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Hypothesis CDK5 Inhibition at Presynaptic Terminals Prevents Activity-Dependent Tau Release and Transsynaptic Propagation rel 4.30

tau levels and a corresponding 35% decrease in tau pathology

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Hypothesis Tau Propagation Blockade via Synaptic Ephrin-B2/ephrin-B Signaling Modulation rel 3.80

tau propagation rests on several converging observations. First, tau pathology

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Hypothesis Autophagic Flux Enhancement Synergizes With Chaperones to Clear High-Molecular-Weight Tau Seeds rel 3.80

tau pathology, p62 accumulates around tau inclusions and facilitates their

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Hypothesis H7: mTOR Hyperactivity Blocks Autophagy, Permitting Tau Seeding rel 3.80

tau-tau interactions and thioflavin-S-positive tau inclusions. Quantitative

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Hypothesis Enhancing Microglial Phagocytosis of Extracellular Tau via TREM2 Activation rel 3.50

tau-positive vesicles and lysosomal markers. The P301S tau transgenic

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Hypothesis Seed Conformational Heterogeneity Explains Variable Chaperone Susceptibility—Strain-Specific Targeting Required rel 3.40

tau conformers within the disease context of protein folding can redirect

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Hypothesis Blocking Tau Packaging into Small Extracellular Vesicles via ESCRT-III Pathway rel 3.00

Tau Packaging into Small Extracellular Vesicles via ESCRT-III Pathway

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Hypothesis Dose-Response Framework: PINK1/Parkin Mitophagy as the Critical Mediator Linking HBOT Parameters to Tau Clearance rel 2.90

tau propagation. When neurons contain mitochondria harboring tau seeds, the PINK1/Parkin

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Hypothesis H1: T-Type Calcium Channel–Driven Calcium Overload and Proteostasis Collapse rel 2.80

tau kinase regulation. Protein phosphatase 2A (PP2A), the primary tau

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Hypothesis TFEB Activation Clears Tau-Loaded Endolysosomal Compartments, Preventing Release for Transcellular Spreading rel 2.80

tau aggregates. [PMID:31320630]. 2. Endolysosomal tau escape in neurons

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Hypothesis Sleep-Dependent Glymphatic Clearance Expands the Therapeutic Window by Reducing Extracellular Tau Burden rel 2.70

tau pathology development and enhanced neuroinflammation. The rTg4510 tau transgenic

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Hypothesis Blocking Exosomal Tau Uptake at Neuronal LRP1 Receptors Disrupts Interneuronal Propagation rel 2.60

tau seeds, and most pathogenic tau transfer may occur via alternative

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Hypothesis Subtle NMDAR Inhibition Attenuates Excitotoxicity-Driven Tau Release from Hypersynchronized Circuits rel 2.60

tau secretion. NMDAR overactivation drives calcium influx and stimulates tau

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Hypothesis CX3CR1 Agonism Enhances Microglial Phagocytosis of Extracellular Tau Seeds, Preventing Template-Dependent Misfolding rel 2.50

tau. CX3CR1 agonism enhances microglial migration to tau deposits, increases

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Hypothesis Soluble GAG-Mimetic Peptides Compete with HSPG for Tau Seed Binding and Prevent Cellular Uptake rel 2.40

tau propagation identified. [PMID:33149142]. 4. Sulfated oligosaccharides inhibit tau

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Hypothesis Targeting Synaptic Vesicle Release Machinery to Block Tau Exocytosis rel 2.40

Tau Exocytosis starts from the claim that Activity-dependent tau

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Hypothesis VPS35 retromer activation prevents endosomal tau templating across all brain regions and disease stages rel 2.30

tau templating across all brain regions and disease stages starts

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Hypothesis Rab27A/B-mediated exosomal tau secretion from microglia drives frontal cortex propagation at Braak III-VI rel 2.30

tau spread in vivo. [PMID:26297806]. 2. Exosomal tau correlates

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Hypothesis LRP1-mediated synaptic uptake drives early entorhinal-hippocampal tau propagation (Braak I-II) rel 2.20

tau propagation (Braak I-II) starts from the claim that

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Hypothesis Disrupting Muscarinic M1/M3 Receptor-Mediated Tau Internalization and Synaptic Targeting rel 2.20

tau phosphorylation at AD-relevant sites and facilitate tau trafficking

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Hypothesis M-Sec/TNTA2-mediated tunneling nanotube formation drives glia-neuron tau propagation in mid-stages rel 2.10

tau propagation in mid-stages starts from the claim that

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Hypothesis Blocking Astrocyte-Mediated Tau Re-Spreading via Cx43 Hemichannel Inhibition rel 2.10

tau through connexin-43 hemichannels and re-release uptake tau

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Hypothesis cGAS-STING Pathway Hyperactivation Mediates Tau Propagation rel 2.00

tau pathology. Functional validation using PS19 tau transgenic mice shows

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Hypothesis Restoring AQP4 Astrocyte Polarization Enhances Glymphatic Tau Clearance and Limits Template-Dependent Spreading rel 1.90

tau may be directional (tau causes mispolarization, not vice versa

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Hypothesis Closed-loop tACS targeting EC-II somatostatin interneurons to restore dendritic integration and prevent tau-mediated HCN channel dysfunction in AD rel 1.80

tau mouse model, tau pathology was sufficient to produce excitatory

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Hypothesis Astrocyte LRP1-mediated tau uptake and APOE4-dependent secretion creates regional susceptibility gradients rel 1.80

tau uptake and APOE4-dependent secretion creates regional susceptibility gradients

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Hypothesis TREM2-Mediated Microglial Dysfunction Drives Tau-Induced Blood-Brain Barrier Breakdown rel 1.80

tau species in perivascular spaces. These accumulated extracellular tau oligomers

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