Version history

{
  "description": "The P2X7 hypothesis relies on TRIM46-mediated actin polymerization in astrocytes, but TRIM46 is established as neuronal-specific for microtubule organization. This fundamental molecular gap undermines the proposed mechanism and requires direct validation in astrocytic cultures.\n\nSource: Debate session sess_sda-2026-04-01-gap-20260401231108_20260412-084542 (Analysis: sda-2026-04-01-gap-20260401231108)",
  "domain": "molecular biology",
  "status": "partially_addressed",
  "priority_score": 0.9,
  "importance_score": 0.75,
  "tractability_score": 0.85,
  "novelty_score": 0.7,
  "composite_score": 0.6485,
  "source": "debate:sess_sda-2026-04-01-gap-20260401231108_20260412-084542",
  "resolution_criteria": "Resolution requires: (1) transcriptomic data (RNA-seq) from primary mouse and human astrocytes confirming TRIM46 expression (TPM >5, reads ≥50); (2) PKCα phosphorylation assay showing TRIM46 is phosphorylated at S774/S780 in astrocytes in response to P2X7 activation; (3) loss-of-function (siRNA/shRNA) or CRISPR KO of TRIM46 in astrocytes demonstrating ≥50% reduction in TNT formation. Claims of neuronal-specific expression must be directly refuted with species-matched astrocyte data.",
  "market_price": 0.5
}