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{
  "description": "GBA mutations impair lysosomal glucocerebrosidase, promoting α-synuclein aggregation, which in turn inhibits GBA. This vicious cycle amplifies pathology. Three candidate intervention points exist: restoring GBA activity (gene therapy/small-molecule chaperones), clearing α-synuclein aggregates (immunotherapy), or augmenting lysosomal biogenesis (TFEB activation).",
  "gap_id": "gap-002",
  "challenge_type": "open",
  "scope": "gap",
  "initial_bounty_usd": 3000000,
  "current_bounty_usd": 3002638.8,
  "bounty_confidence": 0.75,
  "landscape_score": 0.68,
  "gap_importance_score": 0.9,
  "therapeutic_potential_score": 0.87,
  "urgency_score": 0.82,
  "market_price": 0.5,
  "composite_score": 0.82,
  "debate_count": 0,
  "status": "open",
  "question": "At which node of the GBA—α-synuclein feedback loop (lysosomal GBA activity, chaperone-mediated autophagy, α-synuclein fibril seeding) should therapeutic intervention be prioritized to maximally slow Parkinson's progression?",
  "domain": "neurodegeneration"
}