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All 8 Hypotheses 1 Papers 1 Wikis 1 Gaps 1 Colliders 1 Debates 1 Bounties 0 Missions 1 Work packets 1 Genes 0 Diseases 0 Phenotypes 0 Gene ontology 0

+ Hypotheses 1 + Papers 1 + Wikis 1 ✓ Gaps 1 ✓ Colliders 1 + Debates 1 + Bounties 0 + Missions 1 + Work packets 1 + Genes 0 + Diseases 0 + Phenotypes 0 + Gene ontology 0

15 results

Collider Tau-first vs Aβ-first rel 1.00

Posthumous brain-bank readout 2027-Q3 of spatially-resolved tau/Aβ chronology

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Gap Can lysosomal dysfunction convert tau into proteolysis-resistant conformations that propagate independently? rel 0.30

tau seeds was proposed but remains mechanistically unvalidated. This gap prevents

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Gap Does tau dendritic missorting persist independently after Aβ clearance, maintaining neurodegeneration? rel 0.30

tau missorting creates self-sustaining toxicity, but didn't resolve

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Gap Disease-modifying therapies targeting tau pathology beyond anti-amyloid approaches rel 0.20

tau hyperphosphorylation, oligomerization, or propagation remain underdeveloped in the represented

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Gap Does APOE4 drive tau propagation rel 0.20

drive tau propagation [TARGET_ARTIFACT type=hypothesis id=TEST-123]

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Gap Does tau-directed lysosomal rescue alter microglial stress signaling? rel 0.20

Does tau-directed lysosomal rescue alter microglial stress signaling?

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Gap What determines the bidirectional versus unidirectional nature of Aβ-tau synergistic interactions? rel 0.20

tau relationships are bidirectional but didn't resolve what molecular

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Gap What biomarkers can distinguish Aβ-dependent versus Aβ-independent phases of tau pathology progression? rel 0.20

tau toxicity. This knowledge gap prevents patient stratification for precision

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Gap What molecular mechanisms mediate the bidirectional risk between traumatic brain injury and subsequent AD neurodegeneration? rel 0.10

tau pathology years later. Only one trial is actively investigating

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Gap What drives presynaptic glycosyltransferase dysregulation in early AD pathogenesis? rel 0.10

tau, or other factors drive this change is critical for intervention

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Gap Mechanistic understanding of neuroinflammatory pathways in Alzheimer's disease progression rel 0.10

tau pathology, amyloid aggregation, and neuronal loss remain incompletely characterized

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Gap What are the precise inflammatory signaling cascades linking microglial activation to neuronal loss in AD, and can specific nodes be targeted without immunosuppression? rel 0.10

tau aggregation and synaptic loss remain undefined. Current anti-inflammatory

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Gap What combination strategies targeting multiple AD pathogenic pathways (Aβ, tau, inflammation, metabolism) demonstrate disease-modifying efficacy in humans? rel 0.10

No current trials investigate combinatorial approaches. Single-target therapies have

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Gap Epigenetic clocks as biomarkers for Alzheimer disease and neurodegeneration rel 0.10

tau pathology, amyloid burden, alpha-synuclein, TDP-43, and other

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Gap Integrated mechanistic studies of traumatic brain injury as an AD risk factor rel 0.10

Whether TBI accelerates amyloid aggregation, tau seeding, or neuroinflammation remains unresolved.

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