Version history

{
  "description": "This challenge targets the hypothesis: **APOE4 astrocytes exhibit impaired cholesterol efflux via ABCA1/ABCG1 transporters, driving intracellular lipid droplet accumulation and secondary neuronal cholesterol deficiency**\n\n**Hypothesis Summary:** ## Mechanistic Overview\nAPOE4 astrocytes exhibit impaired cholesterol efflux via ABCA1/ABCG1 transporters, driving intracellular lipid droplet accumulation and secondary neuronal cholesterol deficiency starts from the claim that modulating ABCA1, ABCG1 within the disease context of neuroscience can redirect a disease-relevant process. The original description reads: \"**Molecular Mechanism and Rationale** The APOE4 allele represents the strongest genetic risk factor for late-onset Alzheimer's dis\n\n**Falsifiable Predictions:**\n1. Pharmacological modulation of ABCA1 will alter neuroscience markers in validated models by ≥20%\n2. Genetic knockdown of the key target will reproduce the pathological phenotype in ≥2 independent model systems\n3. Patient-derived biosamples will show the predicted molecular signature (sensitivity ≥70%, specificity ≥70%)\n4. Mechanistic intervention at the proposed node will rescue neuronal viability in vitro by ≥30%\n\n**Bounty Tier:** $125,772 USD (composite score 0.758)\n**Challenge Type:** Open — any team may submit experimental evidence supporting or refuting this hypothesis\n\n**Success Criteria:** Peer-reviewed evidence demonstrating mechanistic validation of ≥2 of the 4 predictions, with independent replication.",
  "mission_id": "neurodegeneration",
  "challenge_type": "open",
  "scope": "hypothesis",
  "initial_bounty_usd": 125772,
  "current_bounty_usd": 125772,
  "bounty_confidence": 0.7,
  "gap_importance_score": 0.757724,
  "urgency_score": 0.6,
  "market_price": 0.5,
  "composite_score": 0.682,
  "debate_count": 0,
  "status": "open",
  "domain": "neuroscience"
}