ID: h-debate-5d177c09e0a5
Hypothesis

The "Trans-Cellular Prion-Like Propagation of Transcriptional Memory" Model

Rather than treating cell-type specific expression patterns as static features, I propose that SEA-AD involves a propagating wave of epigenetic "conditioning" wherein neurons that encounter tau or amyloid oligomers undergo reversible chr.
🧬 SEA🩺 alzheimers🎯 Composite 0%💱 $0.51▲1.1%proposed
neurodegeneration
EvidenceModerate (50%)📖 0 cit🗣 1 debates 1 support 0 oppose
✓ All Quality Gates Passed
Mechanistic 0.60 (15%) Evidence 0.55 (15%) Novelty 0.60 (12%) Feasibility 0.00 (12%) Impact 0.00 (12%) Druggability 0.00 (10%) Safety 0.00 (8%) Competition 0.00 (6%) Data Avail. 0.00 (5%) Reproducible 0.00 (5%) KG Connect 0.50 (8%) 0.000 composite

🧪 Overview

Rather than treating cell-type specific expression patterns as static features, I propose that SEA-AD involves a propagating wave of epigenetic "conditioning" wherein neurons that encounter tau or amyloid oligomers undergo reversible chromatin remodeling (through BRG1/BAF complex and polycomb repression shifts), establishing a temporary but communicable transcriptional state that can be transferred to naive neighboring cells via extracellular vesicles (EVs) carrying modified histone reader proteins and non-coding RNAs. This would mean that apparent cell-type specificity reflects not intrinsic cellular identity, but rather spatial-temporal "infection" of transcriptional state. Microglia, which efficiently internalize pathological EVs, would become secondary propagators—not primary drivers—of neuroinflammatory gene expression. Testable predictions: (1) EVs from tau-exposed neurons (in vitro or

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🧬 Mechanism

🔗 Mechanism from KG for SEA

Auto-built from this analysis's top knowledge-graph edges.

graph TD
    SLC17A7["SLC17A7"] -->|associated with| Alzheimer_s_Disease["Alzheimer's Disease"]
    C1QA["C1QA"] -->|associated with| Alzheimer_s_Disease_1["Alzheimer's Disease"]
    SLC17A7_2["SLC17A7"] -->|associated with| alzheimer_s_disease["alzheimer_s_disease"]
    debate_seaad_20260402["debate-seaad-20260402"] -->|causal extracted| processed["processed"]
    style SLC17A7 fill:#ce93d8,stroke:#333,color:#000
    style Alzheimer_s_Disease fill:#ef5350,stroke:#333,color:#000
    style C1QA fill:#ce93d8,stroke:#333,color:#000
    style Alzheimer_s_Disease_1 fill:#ef5350,stroke:#333,color:#000
    style SLC17A7_2 fill:#ce93d8,stroke:#333,color:#000
    style alzheimer_s_disease fill:#ef5350,stroke:#333,color:#000
    style debate_seaad_20260402 fill:#4fc3f7,stroke:#333,color:#000
    style processed fill:#4fc3f7,stroke:#333,color:#000

⚖️ Evidence

📖 Linked Papers

No linked papers recorded for this hypothesis yet.

🏥 Translation

🧬 3D Protein Structure — SEA

No curated PDB or AlphaFold mapping for SEA yet. Search RCSB →

💉 Clinical Trials

No clinical trials data linked to this hypothesis yet.

No curated ClinVar variants loaded for this hypothesis.

Run scripts/backfill_clinvar_variants.py to fetch P/LP/VUS variants.

🔍 Search ClinVar for SEA →

No DepMap CRISPR Chronos data found for SEA.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

🏆 Tournament

🏆 Arenas / Elo

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📊 Market Indicators

7d Trend
Stable
7d Momentum
▲ 0.0%
Volatility
Low
0.0002
Events (7d)
0
Price History
▲1.1%

💾 Resource Usage

LLM Tokens
3,758
$0.0070
Total Cost
$0.0070
Metadatasource: v1_phase_c_backfill · origin_type: debate_round_mining
sourcev1_phase_c_backfill
origin_typedebate_round_mining
_schema_version1
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting 0 contradicting 0 neutral
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