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 neuroinflammation hypotheses, sorted by Composite score.
IL-6 Trans-Signaling Blockade at the Oligodendrocyte-Microglia Interface
IL6R, IL6 neuroinflammation 83%Central IL-6 trans-signaling inhibition reduces neuroinflammation and facilitates recovery from LPS-induced sickness behavior
h-2dbf5f1fPDE4 Inhibition as Inflammatory Reset for PD Oligodendrocytes
PDE4A, PDE4B, PDE4D neuroinflammation 78%53% posterior · 1 signalPDE4 inhibition promotes oligodendrocyte precursor cell differentiation and enhances CNS remyelination
h-67914e81Aryl Hydrocarbon Receptor (AHR) Activation in B Cells Determines AQP4 Tolerance Fate
AHR, IL10, TNFRSF13B, TIGIT, FOXP3 neuroinflammation 74%Microbiota-derived metabolites suppress arthritis by amplifying AHR activation in regulatory B cells
h-ab41908bNLRP3/Mitophagy Coupling Modulation
NLRP3 neuroinflammation 68%53% posterior · 1 signalParkin regulates microglial NLRP3 and represses neurodegeneration in PD
h-f10d82a7C3aR Blockade Disrupts the Microglial-Astrocyte Feedforward Neurotoxic Loop
C3AR1, C3, NFKB1 neuroinflammation 65%53% posterior · 1 signalTranscriptome analysis demonstrates C3/C3aR/NF-κB signaling induces A1 astrocytes after ischemic stroke
h-48b29b62IL-10-Producing B10 Cells Establish AQP4-Specific Peripheral Tolerance Through Macrophage Reprogramming
IL10, CSF1R, CD40 neuroinflammation 65%PubMed search found: Association Between IL10 Polymorphisms and the Susceptibility to Sepsis: A Meta-Analysis.
h-88e23c4aAryl Hydrocarbon Receptor (AhR) Activation by Microbiome Metabolites Promotes A2 Polarization
AHR, CYP1A1, NFKB1, IL6 neuroinflammation 60%53% posterior · 1 signalMicrobiome-derived indole-3-lactic acid reduces amyloidopathy via AhR activation
h-423b50a1TREM2 Signaling Bifurcation with Independent TYROBP-Independent Homeostatic Maintenance
TREM2 neuroinflammation 59%53% posterior · 1 signalTREM2 shedding does not affect inhibition of NFκB activation but completely blocks phagocytosis
h-9c857387Timed Senolytic Therapy Eliminates p16^Ink4a/p21^Cip1-Senescent Microglia to Prevent SASP-Driven Complement Cascade Amplification
CDKN2A (p16^Ink4a), CDKN1A (p21^Cip1/Waf1) neuroinflammation 56%53% posterior · 1 signalSenescent astrocytes and microglia colocalize p16^Ink4a/p21^Cip1/Waf1 at 5 weeks and 4 months post-TBI
h-e14a97bfSYK-Independent TREM2 Pathways Remain Functional in TYROBP Deficiency
SYK, TREM2 neuroinflammation 55%53% posterior · 1 signalTREM2 drives microglia response to amyloid-β via SYK-dependent and -independent pathways
h-69ce9196GAS6/TAM Axis Activation Stabilizes Blood-Brain Barrier to Reduce Neuroinflammatory Cell Infiltration in Alzheimer's Disease
GAS6/TAM receptor complex neuroinflammation 51%MERTK deficiency increases viral neuroinvasion due to BBB breakdown
h-929f356eTYRO3-STAT1 Axis to Preserve Parvalbumin Interneuron Function by Suppressing IL-1β-Mediated Inflammatory Damage
TYRO3 neuroinflammation 51%53% posterior · 1 signalTYRO3 signaling ameliorates IL-1β production through STAT1 in AD models
h-315367deTREM2-SYK Signaling Axis Couples OxPC Recognition to Phagocytic Clearance
TREM2 (Triggering receptor expressed on myeloid cells 2) + SYK (spleen tyrosine kinase) neuroinflammation 45%47% posterior · 1 signalTREM2^high microglia accumulate at OxPC lesions and TREM2^-/- mice exhibit worsened neurodegeneration directly establishing TREM2 as necessary for neuroprotection
h-645cc2deComplement Cascade Activation Bridges Microglial OxPC Sensing to Synaptic Vulnerability
C1QA, C3, C3AR1 (complement cascade) neuroinflammation 42%Established background model links SASP to complement cascade amplification (C1Q/C3, confidence 0.70) providing a foundation mechanism that OxPC pathology would amplify
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