Version history

5 versions on record. Newest first; the live version sits at the top with a live indicator.

  1. Live
    4/27/2026, 6:28:15 PM
    Content snapshot 
    {
  "question": "Does manipulating orexin-A directly rescue cognitive deficits and circadian dysfunction in Alzheimer's disease models?",
  "domain": "neurodegeneration",
  "status": "completed",
  "triggered_by": "codex:aa724961",
  "gap_id": "gap-pubmed-20260410-184240-f72e77ae",
  "metadata": {
    "source": "scripts/generate_3_analyses.py",
    "dissent": [
      "The skeptic noted that orexin-A may worsen rather than rescue cognition in some AD models by increasing wakefulness and amyloid burden.",
      "The expert cautioned that sedating interventions must be separated from disease-modifying effects."
    ],
    "task_id": "aa724961-6a40-495d-9c89-26dadaeda2bd",
    "consensus": [
      "Orexin biology should be tested with time-of-day dosing and sleep/circadian endpoints, not only cognitive behavior.",
      "Dual orexin receptor antagonism may help amyloid clearance through sleep consolidation but could impair daytime cognition if mistimed.",
      "Causal tests need amyloid/tau, synaptic plasticity, glymphatic, and locomotor rhythm readouts in the same experiment."
    ],
    "debate_summary": "The debate framed orexin-A as a bidirectional node linking arousal, sleep fragmentation, glymphatic clearance, synaptic plasticity, and amyloid/tau biology. The synthesis favored temporally controlled orexin receptor modulation over simple orexin-A augmentation or suppression, because timing may determine whether cognition improves or amyloid stress worsens.",
    "world_model_ranking": {
      "formula": "0.30*kg_impact + 0.25*hyp_quality + 0.20*debate_depth + 0.15*gap_addressed + 0.10*research_depth",
      "task_id": "ce3182a7-f33b-44b6-9dd8-ef784cf9e231",
      "weights": {
        "kg_impact": 0.3,
        "hyp_quality": 0.25,
        "debate_depth": 0.2,
        "gap_addressed": 0.15,
        "research_depth": 0.1
      },
      "scored_at": "2026-04-28T01:28:15.062145+00:00",
      "dimension_notes": {
        "kg_impact": "kg_impact_score=0.0 (no direct edge tracking; = 0)",
        "hyp_quality": "avg_composite_score=0.7063 from 3 hypotheses",
        "debate_depth": "avg_debate_quality=0.780 × min(debate_count=1 / 3, 1) = 0.2600",
        "gap_addressed": "gap_id='gap-pubmed-20260410-184240-f72e77ae'",
        "research_depth": "total_hyps_generated=9"
      },
      "dimension_scores": {
        "kg_impact": 0,
        "hyp_quality": 0.706333,
        "debate_depth": 0.26,
        "gap_addressed": 1,
        "research_depth": 0.9
      },
      "world_model_rank": 0.468583
    }
  },
  "world_model_rank": 0.468583,
  "kg_impact_score": 0,
  "completed_at": "2026-04-26T15:23:05.059442-07:00",
  "report_url": "/analyses/SDA-2026-04-26-gap-pubmed-20260410-184240-f72e77ae",
  "reproducibility_class": "observational"
}
  2. v4
    4/26/2026, 3:23:05 PM
    Content snapshot 
    {
  "question": "Does manipulating orexin-A directly rescue cognitive deficits and circadian dysfunction in Alzheimer's disease models?",
  "domain": "neurodegeneration",
  "status": "completed",
  "triggered_by": "codex:aa724961",
  "gap_id": "gap-pubmed-20260410-184240-f72e77ae",
  "metadata": {
    "source": "scripts/generate_3_analyses.py",
    "dissent": [
      "The skeptic noted that orexin-A may worsen rather than rescue cognition in some AD models by increasing wakefulness and amyloid burden.",
      "The expert cautioned that sedating interventions must be separated from disease-modifying effects."
    ],
    "task_id": "aa724961-6a40-495d-9c89-26dadaeda2bd",
    "consensus": [
      "Orexin biology should be tested with time-of-day dosing and sleep/circadian endpoints, not only cognitive behavior.",
      "Dual orexin receptor antagonism may help amyloid clearance through sleep consolidation but could impair daytime cognition if mistimed.",
      "Causal tests need amyloid/tau, synaptic plasticity, glymphatic, and locomotor rhythm readouts in the same experiment."
    ],
    "debate_summary": "The debate framed orexin-A as a bidirectional node linking arousal, sleep fragmentation, glymphatic clearance, synaptic plasticity, and amyloid/tau biology. The synthesis favored temporally controlled orexin receptor modulation over simple orexin-A augmentation or suppression, because timing may determine whether cognition improves or amyloid stress worsens."
  },
  "completed_at": "2026-04-26T15:23:05.059442-07:00",
  "report_url": "/analyses/SDA-2026-04-26-gap-pubmed-20260410-184240-f72e77ae"
}
  3. v3
    4/26/2026, 3:23:05 PM
    Content snapshot 
    {
  "question": "Does manipulating orexin-A directly rescue cognitive deficits and circadian dysfunction in Alzheimer's disease models?",
  "domain": "neurodegeneration",
  "status": "completed",
  "triggered_by": "codex:aa724961",
  "gap_id": "gap-pubmed-20260410-184240-f72e77ae",
  "metadata": {
    "source": "scripts/generate_3_analyses.py",
    "dissent": [
      "The skeptic noted that orexin-A may worsen rather than rescue cognition in some AD models by increasing wakefulness and amyloid burden.",
      "The expert cautioned that sedating interventions must be separated from disease-modifying effects."
    ],
    "task_id": "aa724961-6a40-495d-9c89-26dadaeda2bd",
    "consensus": [
      "Orexin biology should be tested with time-of-day dosing and sleep/circadian endpoints, not only cognitive behavior.",
      "Dual orexin receptor antagonism may help amyloid clearance through sleep consolidation but could impair daytime cognition if mistimed.",
      "Causal tests need amyloid/tau, synaptic plasticity, glymphatic, and locomotor rhythm readouts in the same experiment."
    ],
    "debate_summary": "The debate framed orexin-A as a bidirectional node linking arousal, sleep fragmentation, glymphatic clearance, synaptic plasticity, and amyloid/tau biology. The synthesis favored temporally controlled orexin receptor modulation over simple orexin-A augmentation or suppression, because timing may determine whether cognition improves or amyloid stress worsens."
  },
  "completed_at": "2026-04-26T15:23:05.059442-07:00",
  "report_url": "/analyses/SDA-2026-04-26-gap-pubmed-20260410-184240-f72e77ae"
}
  4. v2
    4/26/2026, 3:23:05 PM
    Content snapshot 
    {
  "question": "Does manipulating orexin-A directly rescue cognitive deficits and circadian dysfunction in Alzheimer's disease models?",
  "domain": "neurodegeneration",
  "status": "completed",
  "triggered_by": "codex:aa724961",
  "gap_id": "gap-pubmed-20260410-184240-f72e77ae",
  "metadata": {
    "source": "scripts/generate_3_analyses.py",
    "dissent": [
      "The skeptic noted that orexin-A may worsen rather than rescue cognition in some AD models by increasing wakefulness and amyloid burden.",
      "The expert cautioned that sedating interventions must be separated from disease-modifying effects."
    ],
    "task_id": "aa724961-6a40-495d-9c89-26dadaeda2bd",
    "consensus": [
      "Orexin biology should be tested with time-of-day dosing and sleep/circadian endpoints, not only cognitive behavior.",
      "Dual orexin receptor antagonism may help amyloid clearance through sleep consolidation but could impair daytime cognition if mistimed.",
      "Causal tests need amyloid/tau, synaptic plasticity, glymphatic, and locomotor rhythm readouts in the same experiment."
    ],
    "debate_summary": "The debate framed orexin-A as a bidirectional node linking arousal, sleep fragmentation, glymphatic clearance, synaptic plasticity, and amyloid/tau biology. The synthesis favored temporally controlled orexin receptor modulation over simple orexin-A augmentation or suppression, because timing may determine whether cognition improves or amyloid stress worsens."
  },
  "completed_at": "2026-04-26T15:23:05.059442-07:00",
  "report_url": "/analyses/SDA-2026-04-26-gap-pubmed-20260410-184240-f72e77ae"
}
  5. v1
    4/26/2026, 3:23:05 PM
    Content snapshot 
    {
  "question": "Does manipulating orexin-A directly rescue cognitive deficits and circadian dysfunction in Alzheimer's disease models?",
  "domain": "neurodegeneration",
  "status": "completed",
  "triggered_by": "codex:aa724961",
  "gap_id": "gap-pubmed-20260410-184240-f72e77ae",
  "metadata": {
    "source": "scripts/generate_3_analyses.py",
    "dissent": [
      "The skeptic noted that orexin-A may worsen rather than rescue cognition in some AD models by increasing wakefulness and amyloid burden.",
      "The expert cautioned that sedating interventions must be separated from disease-modifying effects."
    ],
    "task_id": "aa724961-6a40-495d-9c89-26dadaeda2bd",
    "consensus": [
      "Orexin biology should be tested with time-of-day dosing and sleep/circadian endpoints, not only cognitive behavior.",
      "Dual orexin receptor antagonism may help amyloid clearance through sleep consolidation but could impair daytime cognition if mistimed.",
      "Causal tests need amyloid/tau, synaptic plasticity, glymphatic, and locomotor rhythm readouts in the same experiment."
    ],
    "debate_summary": "The debate framed orexin-A as a bidirectional node linking arousal, sleep fragmentation, glymphatic clearance, synaptic plasticity, and amyloid/tau biology. The synthesis favored temporally controlled orexin receptor modulation over simple orexin-A augmentation or suppression, because timing may determine whether cognition improves or amyloid stress worsens."
  },
  "completed_at": "2026-04-26T15:23:05.059442-07:00"
}