Hypothesis corpus
Scored, debated, and tradable. Each hypothesis carries composite, novelty, impact, mechanistic, druggability, and safety scores — plus a live market price when a collider is open.
Showing Alzheimer's Disease hypotheses, sorted by Composite score.
ACSL4-Driven Ferroptotic Priming in Disease-Associated Microglia
ACSL4 Alzheimer's Disease 89%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-seaad-v4-26ba859bACSL4-Ferroptotic Priming in Stressed Oligodendrocytes Drives White Matter Degeneration in Alzheimer's Disease
ACSL4 Alzheimer's Disease 80%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-var-22c38d11cd40 Hz Gamma Entrainment Gates ACSL4-Mediated Ferroptotic Priming to Selectively Eliminate Disease-Associated Microglia
ACSL4 Alzheimer's Disease 80%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-var-261452bfb4ACSL4-Driven Ferroptotic Priming in Disease-Associated Oligodendrocytes Underlies White Matter Degeneration in Alzheimer's Disease
ACSL4 Alzheimer's Disease 78%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-var-f96e38ec20LPCAT3-Mediated Lands Cycle Remodeling as the Primary Ferroptotic Priming Engine in Disease-Associated Microglia
LPCAT3 Alzheimer's Disease 78%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-var-e4cae9d286LPCAT3-Mediated Lands Cycle Amplification of Ferroptotic Substrate Pools in Disease-Associated Microglia
LPCAT3 Alzheimer's Disease 78%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-var-c56b26facfALOX15-Driven Enzymatic Ferroptosis in AD Oligodendrocytes via PUFA-PE Peroxidation
ALOX15 Alzheimer's Disease 77%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-var-97b18b880dLPCAT3-Mediated Lands Cycle Amplification of Ferroptotic Vulnerability in Disease-Associated Microglia
LPCAT3 Alzheimer's Disease 76%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-var-70a95f9d57Cell-Type Specific TREM2 Upregulation in DAM Microglia
TREM2 Alzheimer's Disease 76%TREM2 is upregulated in DAM microglia near amyloid plaques
h-seaad-51323624GFAP-Positive Reactive Astrocyte Subtype Delineation
GFAP Alzheimer's Disease 75%Plasma GFAP predicts AD pathology and cognitive decline
h-seaad-56fa6428APOE Isoform Expression Across Glial Subtypes
APOE Alzheimer's Disease 74%APOE4 is the strongest genetic risk factor for late-onset AD
h-seaad-fa5ea82dSIRT3-Mediated Mitochondrial Deacetylation Failure with PINK1/Parkin Mitophagy Dysfunction
SIRT3 Alzheimer's Disease 74%SIRT3 deacetylates mitochondrial proteins essential for oxidative phosphorylation and ROS defense
h-seaad-v4-5a7a4079Complement C1QA Spatial Gradient in Cortical Layers
C1QA Alzheimer's Disease 68%C1q mediates synapse loss in AD mouse models
h-seaad-5b3cb8eaExcitatory Neuron Vulnerability via SLC17A7 Downregulation
SLC17A7 Alzheimer's Disease 67%VGLUT1 protein levels decrease early in AD temporal cortex
h-seaad-7f15df4cAstrocyte MCT1/MCT4 Ratio Disruption with Metabolic Uncoupling
SLC16A1 Alzheimer's Disease 67%Astrocyte-neuron lactate shuttle provides critical metabolic support for synaptic plasticity and memory
h-seaad-v4-29e81bbcTREM2-mediated microglial tau clearance enhancement
TREM2 Alzheimer's Disease 62%TREM2 maintains microglial metabolic fitness; deficiency causes mitochondrial dysfunction and impaired phagocytosis
h-b234254cLRP1-Dependent Tau Uptake Disruption
LRP1 Alzheimer's Disease 60%LRP1 is a neuronal receptor for α-synuclein uptake and spread.
h-4dd0d19bVCP-Mediated Autophagy Enhancement
VCP Alzheimer's Disease 59%Mitochondria ROS and mitophagy in acute kidney injury.
h-18a0fcc6Extracellular Vesicle Biogenesis Modulation
CHMP4B Alzheimer's Disease 58%ALIX- and ESCRT-III-dependent sorting of tetraspanins to exosomes.
h-55ef81c5Synaptic Vesicle Tau Capture Inhibition
SNAP25 Alzheimer's Disease 58%Common Mechanism Underlying Synaptic Dysfunction Caused by Preformed Fibril-Induced Accumulation of α-Synuclein or Tau in a Culture Propagation Model.
h-73e29e3aHSP90-Tau Disaggregation Complex Enhancement
HSP90AA1 Alzheimer's Disease 57%HSP90 interacts with tau and modulates its folding, aggregation, and degradation
h-0f00fd75Trans-Synaptic Adhesion Molecule Modulation
NLGN1 Alzheimer's Disease 54%Membrane trafficking of synaptic adhesion molecules.
h-fdaae8d9ACSL4-Mediated Neuroinflammatory Amplification in Disease-Associated Microglia
ACSL4 Alzheimer's Disease 46%ACSL4 shapes cellular lipid composition to trigger ferroptosis through PUFA-PE enrichment
h-var-c4c7aca6dcMicroglia-mediated antigen presentation creates a peripheral sink for tau antibodies
Alzheimer's Disease 0%Mechanistic rationale: Fcγ receptor-mediated phagocytosis of antibody-opsonized tau targets tau to microglial lysosomes. While this may reduce extracellular tau, it simultaneously triggers microglial…
h-debate-829763a5efc0