Version history

{
  "description": "The debate implied therapeutic windows exist but didn't identify how to detect transition points between Aβ-dependent and independent tau toxicity. This knowledge gap prevents patient stratification for precision medicine approaches targeting synergistic mechanisms.\n\nSource: Debate session sess_SDA-2026-04-16-gap-pubmed-20260410-180503-a7a03974_20260416-134419 (Analysis: SDA-2026-04-16-gap-pubmed-20260410-180503-a7a03974)",
  "domain": "biomarker development",
  "status": "open",
  "priority_score": 0.85,
  "importance_score": 0.92,
  "tractability_score": 0.75,
  "novelty_score": 0.8,
  "composite_score": 0.7191,
  "estimated_effort": "high",
  "source": "debate:sess_SDA-2026-04-16-gap-pubmed-20260410-180503-a7a03974_20260416-134419",
  "resolution_criteria": "Resolved when a biomarker panel distinguishes Abeta-dependent from Abeta-independent tau progression phases in longitudinal AD cohorts. Required evidence: amyloid PET, tau PET, plasma/CSF p-tau species, NfL, GFAP, and cognition modeled over time with change-point or mediation analysis. Closure requires validated thresholds that predict when tau accumulation continues despite stable/low amyloid burden, with replication in an independent cohort or trial dataset.",
  "market_price": 0.5
}