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30 results

Hypothesis TREM2-Mediated Microglial Dysfunction Impairs Synaptic Tau Propagation Blockade rel 1.50

tau oligomers released from presynaptic terminals through direct binding to tau

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Hypothesis Alpha-theta entrainment therapy to enhance default mode network coherence rel 1.40

Alpha-theta entrainment therapy targets somatostatin (SST) interneurons to restore

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Hypothesis Synaptic Vesicle Cycle Hijacking: Shared Convergent Mechanism for α-Synuclein (PD) and Tau (AD) Trans-synaptic Propagation rel 1.10

tau (MAPT) in Alzheimer's disease exploit the same synaptic

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Hypothesis GluN2B-Mediated Microglial Activation and Tau Phagocytosis rel 0.80

tau protein clearance through enhanced phagocytic activity rather than glymphatic

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Hypothesis Repeat-domain exposure defines seed-competent tau conformers rel 0.80

tau conformations. Non-pathogenic transferred tau lacks this exposed templating

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Hypothesis Epigenetic Age Acceleration Moderates the Amyloid-to-Tau Conversion Cascade — A "Clock Threshold" Model of AD Progression rel 0.70

tau propagation becomes dramatically accelerated, explaining the highly variable lag between

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Hypothesis Real-time optogenetic activation of CA3 PV interneurons to restore theta-gamma coupling and prevent synaptic tau accumulation in AD rel 0.60

tau phosphorylation and prevents tau accumulation at CA3-CA1 Schaffer

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Hypothesis Enhancing Heparan Sulfate 3-O-Sulfotransferase Activity to Competitively Block Tau-HSPG Interactions rel 0.60

tau aggregates in Alzheimer's disease relies critically on heparan

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Hypothesis Closed-loop transcranial focused ultrasound to restore hippocampal gamma oscillations via SST interneuron disinhibition cascades in Alzheimer's disease rel 0.60

This intervention targets somatostatin-positive (SST) interneurons in the stratum

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Hypothesis O-GlcNAcylation at T212 competes with phosphorylation to redirect pathological tau from ESCRT-dependent exosomal release rel 0.60

tau's abnormal interaction with the ESCRT machinery for exosomal

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Hypothesis Closed-loop transcranial focused ultrasound with gamma entrainment to restore hippocampal-cortical synchrony via PV interneuron mechanostimulation rel 0.60

This hypothesis combines the precision of transcranial focused ultrasound (tFUS

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Hypothesis A tau PTM barcode gates trans-synaptic templating rel 0.50

convert seed-competent tau into transferable but weakly pathogenic tau.

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Hypothesis Lysosomal Acidification Failure: Convergent GBA1/LAMP2A–mediated Autophagy Dysfunction Links PD and AD Clinical Progression rel 0.50

tau blocks LAMP2A → tau accumulates → more tau blocks LAMP2A. Additionally

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Hypothesis SULF-Mediated Protection of Cholinergic Tau Transport Pathways rel 0.50

tau uptake and preserving intracellular cholinergic function. The molecular mechanism

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Hypothesis Axonal Integrity Recovery Following Amyloid Clearance Drives CSF p-tau217 Normalization rel 0.50

tau fragments and hyperphosphorylated tau species into CSF. However, this

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Hypothesis Dopaminergic Ventral Tegmental-Striatal Circuit Protection rel 0.50

tau protein dysfunction specifically compromises dopaminergic neurotransmission through disrupted axonal

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Hypothesis Competitive Co-chaperone Displacement rel 0.40

tau-stabilizing immunophilins (FKBP51) from HSP90 while recruiting tau-destabilizing

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Hypothesis TREM2-Regulated Astrocytic Calcium Dynamics Control Glymphatic Tau Clearance rel 0.40

tau clearance efficiency. The mechanism begins with TREM2/DAP12 signaling in perivascular

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Hypothesis HSP90-cochaperone complexes preferentially stabilize intermediate misfolded states preceding amyloid formation rel 0.40

The HSP90 chaperone system, comprising HSP90AA1 and HSP90AB1 in complex

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Hypothesis PINK1/Parkin–TREM2 Axis: Convergent Mitophagy Failure Unifies PD (SNCA/αSyn) and AD (tau/Abeta) Pathology rel 0.40

tau (MAPT) via GSK3B activation and drives amyloid-beta (APP/ABCA1

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Hypothesis Heparan sulfate proteoglycan binding selectivity determines misfolded protein transmission efficiency rel 0.40

tau, α-synuclein, TDP-43) is determined by their distinct

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Hypothesis NRF2-Mediated Proteostatic Convergence: Shared Oxidative Stress Response Failure Links PD (SNCA Aggregation) and AD (Abeta/Tau Accumulation) rel 0.40

tau (via GSK3B) both suppress NRF2 transcription and promote KEAP1

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Hypothesis Endosomal escape determines whether transferred tau becomes pathogenic rel 0.40

tau species are transferred between neurons but remain non-pathogenic

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Hypothesis J-protein substrate specificity codes enable HSP70 discrimination of β-sheet versus α-helical misfolded conformers rel 0.40

The HSP70 chaperone system achieves selective recognition of pathogenic protein

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Hypothesis MAP6-mediated microtubule stabilization as therapeutic target rel 0.30

tau-independent cytoskeletal defects in neurodegeneration, and stabilizing MAP6-microtubule

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Hypothesis Tau Conformational Change-Triggered Membrane Disruption rel 0.30

tau conformational epitopes and simultaneously possess membrane-disrupting activity could

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Hypothesis Glycan-Targeting Tau Vesicle Interceptors rel 0.30

Tau-containing vesicles display aberrant sialylation patterns that can be targeted

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Hypothesis Glycan-Disrupting Tau Disaggregation rel 0.30

tau vesicle surfaces using targeted glycosidases could disrupt the molecular

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Hypothesis TFEB Activation to Restore Lysosomal Biogenesis in Alzheimer's Disease Neuronal Networks rel 0.30

tau tangles that disrupt synaptic transmission and neuronal survival. This

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Hypothesis Allosteric Pocket Exploitation for Tau-Specific HSP90 Modulation rel 0.30

tau-containing complexes, selectively destabilizing tau-HSP90 interactions while preserving

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