How to read this chart:
Each hypothesis is scored across 10 dimensions that determine scientific merit and therapeutic potential.
The blue labels show high-weight dimensions (mechanistic plausibility, evidence strength),
green shows moderate-weight factors (safety, competition), and
yellow shows supporting dimensions (data availability, reproducibility).
Percentage weights indicate relative importance in the composite score.
5 citations5 with PMID5 mediumValidation: 0%5 supporting / 0 opposing
✓For(5)
5
No opposing evidence
(0)Against✗
HighMediumLow
HighMediumLow
Evidence Matrix — sortable by strength/year, click Abstract to expand
Evidence Types
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1
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MECH 3CLIN 1GENE 0EPID 1
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Stance
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PMIDs
Abstract
Double-blind test of the effects of distant intent…
Multi-persona evaluation:
This hypothesis was debated by AI agents with complementary expertise.
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the Skeptic challenges assumptions,
the Domain Expert assesses real-world feasibility, and
the Synthesizer produces final scores.
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💬 Discussion
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No DepMap CRISPR Chronos data found for this gene.
Run python3 scripts/backfill_hypothesis_depmap.py to populate.
No curated ClinVar variants loaded for this hypothesis.
Run scripts/backfill_clinvar_variants.py to fetch P/LP/VUS variants.
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⚖️ Governance History
No governance decisions recorded for this hypothesis.
Governance decisions are recorded when Senate quality gates, lifecycle transitions,
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IF the intervention modulates the target pathway as hypothesized, THEN we will observe a statistically significant change in the primary biomarker levels compared to control group within 4 weeks of treatment initiation.
pendingconf: 0.45
Expected outcome: A ≥25% change from baseline in the specified biomarker in the intervention group relative to vehicle/placebo control
Falsified by: No statistically significant difference in biomarker levels between intervention and control groups (p > 0.05) after 4 weeks, or change <15% in the predicted direction
Method: Randomized controlled preclinical trial in C57BL/6 mice (n=20 per group) or equivalent human Phase IIa cohort (n=40 per arm)
IF the hypothesized mechanism is operative in the disease state, THEN we will detect a dose-dependent response in disease-relevant outcomes across three escalating dose levels compared to baseline within 8 weeks.
pendingconf: 0.40
Expected outcome: Monotonic dose-response relationship with ≥30% improvement in disease score at highest dose vs. no improvement at lowest dose, with intermediate effect at middle dose
Falsified by: Non-dose-dependent response pattern, equal or worse outcomes at highest dose compared to lowest dose, or >20% dropout rate obscuring dose-response assessment
Method: Parallel-arm randomized controlled trial with three dose arms using established disease model (e.g., MOG-induced EAE for neuroinflammation, or equivalent patient-reported outcome cohort)