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Hypothesis portfolio targeting amyloid-beta, tau, microglial priming, and lipid metabolism in AD. Biggest v1 corpus segment with ~310 scored hypotheses; the v2 mission re-binds them via typed substrate links (SPEC-027 §5) instead of v1's hypothesis_missions junction table.

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

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Does tau-directed lysosomal rescue alter microglial stress signaling?

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

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

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

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

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tau pathology years later. Only one trial is actively investigating

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

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