Version history

{
  "description": "Anti-amyloid antibodies achieve only ~0.1% brain penetrance via passive diffusion, limiting efficacy. Receptor-mediated transcytosis approaches (TfR1, LRP1) have shown 10-20x improvements in rodents but often fail in NHP due to target expression differences. Novel strategies (pH-sensitive unbinding, exosome loading) require systematic evaluation.",
  "gap_id": "gap-008",
  "challenge_type": "open",
  "scope": "gap",
  "initial_bounty_usd": 5000000,
  "current_bounty_usd": 5008097.399999999,
  "bounty_confidence": 0.82,
  "landscape_score": 0.78,
  "gap_importance_score": 0.95,
  "therapeutic_potential_score": 0.93,
  "urgency_score": 0.9,
  "market_price": 0.5,
  "composite_score": 0.89,
  "debate_count": 0,
  "status": "open",
  "question": "What molecular shuttle strategy — transferrin receptor, LRP1, novel pH-responsive linkers, or engineered exosome vectors — achieves >1% brain penetrance for therapeutic antibodies while maintaining target specificity?",
  "domain": "neurodegeneration"
}