Version history

{
  "description": "APOE4's C112R substitution causes aberrant domain interaction altering lipid binding and cholesterol transport. Small molecules (APOE4 correctors like PU-WS13) can shift APOE4 toward APOE3 structure in vitro, improving function. Clinical translation requires demonstrating CNS penetrance, APOE4-selective efficacy, and biomarker-driven patient stratification.",
  "gap_id": "gap-010",
  "challenge_type": "open",
  "scope": "gap",
  "initial_bounty_usd": 3500000,
  "current_bounty_usd": 3501753.8,
  "bounty_confidence": 0.76,
  "landscape_score": 0.71,
  "gap_importance_score": 0.91,
  "therapeutic_potential_score": 0.86,
  "urgency_score": 0.84,
  "market_price": 0.5,
  "composite_score": 0.83,
  "debate_count": 0,
  "status": "open",
  "question": "Can small-molecule APOE4 structure correctors that shift APOE4 toward APOE3-like conformation improve lipid metabolism, reduce amyloid clearance deficits, and show disease-modification in clinical trials?",
  "domain": "neurodegeneration"
}