Version history
1 version on record. Newest first; the live version sits at the top with a live indicator.
- Live4/26/2026, 3:23:04 PM
Content snapshot
{ "session_id": "sess_SDA-2026-04-26-gap-debate-20260412-094623-bb7e1c4f_task-aa724961", "round_number": 1, "agent_persona": "persona-theorist", "agent_backend": "codex-curated", "action": "propose", "content": "Seed-competent tau is likely defined by a compact beta-rich conformer exposing repeat-domain surfaces, a permissive PTM barcode, and packaging into vesicles or synaptic compartments that protect it from degradation during transfer.", "hypotheses_referenced": "[\"Repeat-domain exposure defines seed-competent tau conformers\", \"A tau PTM barcode gates trans-synaptic templating\", \"Endosomal escape determines whether transferred tau becomes pathogenic\"]", "evidence_cited": "[\"Seed competence must be defined functionally by templating kinetics, not only by aggregate size or uptake.\", \"Phosphorylation, acetylation, truncation, and ubiquitin-adaptor context are likely to gate which tau assemblies survive transfer and template.\", \"Blocking pathogenic transfer should preserve physiological tau and general exosome biology where possible.\"]", "tokens_used": "57", "persona_id": "persona-theorist", "confidence": 0.72, "argument": "Seed-competent tau is likely defined by a compact beta-rich conformer exposing repeat-domain surfaces, a permissive PTM barcode, and packaging into vesicles or synaptic compartments that protect it from degradation during transfer.", "evidence": "{\"consensus\": [\"Seed competence must be defined functionally by templating kinetics, not only by aggregate size or uptake.\", \"Phosphorylation, acetylation, truncation, and ubiquitin-adaptor context are likely to gate which tau assemblies survive transfer and template.\", \"Blocking pathogenic transfer should preserve physiological tau and general exosome biology where possible.\"], \"dissent\": [\"The skeptic argued that many observed tau strains may be assay artifacts unless validated across PMCA, RT-QuIC, FRET biosensor, and in vivo spread systems.\", \"The expert noted that conformation-specific biologics need biomarkers that identify patients with the target strain.\"]}" }