Version history

{
  "description": "Falsifiable prediction from high-scoring hypothesis (score=0.720, gene=NLRP3/CASP1/IL1B). Hypothesis: Does the NLRP3 inflammasome enter a locked 'hyperactive' state in senescent astrocytes that perpetuates the senescence-associated inflammasome phenotype (SASP), and does MCC950 (NLRP3 inhibitor) break this lock to reduce neuroinflammation in AD? Success criteria: 1. MCC950 (10mg/kg, 4 weeks) reduces IBA1+/CD68+ microglia by >40% in 5xFAD mice vs vehicle. 2. Senescent astrocyte marker (p16^INK4a) colocalization with NLRP3 decreases by >50% after MCC950. 3. SASP factors (IL-6, CXCL1) in CSF decrease by >35% in MCC950-treated 5xFAD mice. 4. Cognitive performance (Morris water maze) improves by >25% vs vehicle controls.",
  "challenge_type": "hypothesis_resolve",
  "scope": "single_target",
  "initial_bounty_usd": 250,
  "current_bounty_usd": 250,
  "bounty_confidence": 0.3,
  "market_price": 0.5,
  "composite_score": 0.72,
  "debate_count": 0,
  "status": "open",
  "question": "Does the NLRP3 inflammasome enter a locked 'hyperactive' state in senescent astrocytes that perpetuates the senescence-associated inflammasome phenotype (SASP), and does MCC950 (NLRP3 inhibitor) break this lock to reduce neuroinflammation in AD?",
  "domain": "neurodegeneration",
  "triggered_by": "hypothesis-auto-create"
}