AD fine-mapping identifies causal variants in microglia-specific enhancers with small credible sets

Target: TREM2 Composite Score: 0.000 Price: $0.50▲52.0% Citation Quality: Pending Alzheimer's disease Status: proposed
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✓ All Quality Gates Passed
Evidence Strength Pending (0%)
5
Citations
1
Debates
5
Supporting
2
Opposing
Quality Report Card click to collapse
F
Composite: 0.000
Top 50% of 1512 hypotheses
T4 Speculative
Novel AI-generated, no external validation
Needs 1+ supporting citation to reach Provisional
A Mech. Plausibility 15% 0.86 Top 12%
B+ Evidence Strength 15% 0.72 Top 19%
B Novelty 12% 0.68 Top 54%
A Feasibility 12% 0.85 Top 18%
F Impact 12% 0.00 Top 50%
F Druggability 10% 0.00 Top 50%
F Safety Profile 8% 0.00 Top 50%
F Competition 6% 0.00 Top 50%
F Data Availability 5% 0.00 Top 50%
F Reproducibility 5% 0.00 Top 50%
Evidence
5 supporting | 2 opposing
Citation quality: 42%
Debates
2 sessions B
Avg quality: 0.65
Convergence
0.00 F 30 related hypothesis share this target

From Analysis:

Statistical Fine-Mapping of AD GWAS Loci to Identify Causal Variants

Can Bayesian fine-mapping of the top 25 AD GWAS loci identify credible sets of causal variants with high posterior probability?

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Description

Bayesian fine-mapping of the top 25 AD GWAS loci will identify credible sets significantly enriched for variants disrupting microglia-specific regulatory elements, reflecting microglial dysfunction as a central AD pathogenic mechanism. Credible sets at loci with known effector genes (APOE, TREM2, PLCG2) will be smaller (<10 variants) due to stronger functional constraints, while novel loci will have larger sets requiring integration with epigenomic data to prioritize causal variants. The highest posterior probability variants will predominantly map to non-coding regulatory regions active in myeloid cells rather than neuronal or astrocytic enhancers.

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Dimension Scores

How to read this chart: Each hypothesis is scored across 10 dimensions that determine scientific merit and therapeutic potential. The blue labels show high-weight dimensions (mechanistic plausibility, evidence strength), green shows moderate-weight factors (safety, competition), and yellow shows supporting dimensions (data availability, reproducibility). Percentage weights indicate relative importance in the composite score.
Mechanistic 0.86 (15%) Evidence 0.72 (15%) Novelty 0.68 (12%) Feasibility 0.85 (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
7 citations 7 with PMID 5 medium Validation: 42% 5 supporting / 2 opposing
For (5)
5
No opposing evidence
(2) Against
High Medium Low
High Medium Low
Evidence Matrix — sortable by strength/year, click Abstract to expand
Evidence Types
5
2
MECH 5CLIN 0GENE 2EPID 0
ClaimStanceCategorySourceStrength ↕Year ↕Quality ↕PMIDsAbstract
PubMed PMID 36306735SupportingMECHPubMed MEDIUM--PMID:36306735-
PubMed PMID 33516818SupportingMECHPubMed MEDIUM--PMID:33516818-
PubMed PMID 28602351SupportingMECHPubMed MEDIUM--PMID:28602351-
PubMed PMID 38821351SupportingMECHPubMed MEDIUM--PMID:38821351-
PubMed PMID 32579671SupportingMECHPubMed MEDIUM--PMID:32579671-
Systematic CRISPRi fine-mapping of AD GWAS loci re…OpposingGENE- STRONG--PMID:41427057-
Genetic drivers of Alzheimer's disease progre…OpposingGENE- MODERATE--PMID:41332834-
Legacy Card View — expandable citation cards

Supporting Evidence 5

PubMed PMID 36306735 MEDIUM
PubMed · PMID:36306735
PubMed PMID 33516818 MEDIUM
PubMed · PMID:33516818
PubMed PMID 28602351 MEDIUM
PubMed · PMID:28602351
PubMed PMID 38821351 MEDIUM
PubMed · PMID:38821351
PubMed PMID 32579671 MEDIUM
PubMed · PMID:32579671

Opposing Evidence 2

Systematic CRISPRi fine-mapping of AD GWAS loci reveals heterogeneous causal cell types across loci; multiple … STRONG
Systematic CRISPRi fine-mapping of AD GWAS loci reveals heterogeneous causal cell types across loci; multiple risk genes implicate non-microglial mechanisms including neuronal and oligodendrocyte functions, challenging the prediction that most AD loci harbour microglia-specific enhancer variants
Genetic drivers of Alzheimer's disease progression are largely distinct from disease-risk loci and involve neu… MODERATE
Genetic drivers of Alzheimer's disease progression are largely distinct from disease-risk loci and involve neuronal pathways; this dichotomy suggests that relying on risk GWAS loci to infer microglial-enhancer causality may miss substantial non-microglial genetic architecture
Multi-persona evaluation: This hypothesis was debated by AI agents with complementary expertise. The Theorist explores mechanisms, the Skeptic challenges assumptions, the Domain Expert assesses real-world feasibility, and the Synthesizer produces final scores. Expand each card to see their arguments.
Gap Analysis | 4 rounds | 2026-04-21 | View Analysis
🧬 Theorist Proposes novel mechanisms and generates creative hypotheses

[Error in hypothesis generation: complete() got an unexpected keyword argument 'tools']

🔍 Skeptic Identifies weaknesses, alternative explanations, and methodological concerns

Critical Evaluation of AD Fine-Mapping Hypotheses

Hypothesis 1: Strong LD Enables Narrow Credible Sets

Weaknesses

The fundamental problem with this hypothesis is a category error: strong LD is a hindrance, not a help, for variant-level resolution. When variants are highly correlated, posterior probability diffuses across the LD block, making pinpointing the causal variant statistically harder, not easier. The hypothesis conflates "high statistical power to detect association" with "narrow credible sets."

The APOE/TOMM40 region is particularly problematic as an exemplar. De

🎯 Domain Expert Assesses practical feasibility, druggability, and clinical translation

[Error in expert assessment: complete() got an unexpected keyword argument 'tools']

Synthesizer Integrates perspectives and produces final ranked assessments

{"ranked_hypotheses":[],"synthesis_summary":"Synthesis could not be completed due to errors in receiving inputs from component agents. The Theorist, Skeptic, and Expert modules all returned errors stating 'complete() got an unexpected keyword argument tools', indicating a technical issue with agent invocation. Without validated hypotheses, critique, or feasibility assessments, no ranking or synthesis can be produced. Please verify the agent configuration and retry the generation pipeline.","knowledge_edges":[]}

Price History

0.550.630.71 0.78 0.48 2026-04-262026-04-272026-04-27 Market PriceScoreevidencedebate 2 events
7d Trend
Stable
7d Momentum
▲ 52.0%
Volatility
Low
0.0000
Events (7d)
2

Clinical Trials (0)

No clinical trials data available

📚 Cited Papers (7)

No extracted figures yet
No extracted figures yet
TREM2, microglia, and Alzheimer's disease.
Mech Ageing Dev (2021) · PMID:33516818
No extracted figures yet
No extracted figures yet
Microglia and TREM2.
Neuropharmacology (2024) · PMID:38821351
No extracted figures yet
No extracted figures yet
No extracted figures yet

📙 Related Wiki Pages (0)

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⚔ Arena Performance

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📊 Resource Economics & ROI

Moderate Efficiency Resource Efficiency Score
0.50
32.3th percentile (776 hypotheses)
Tokens Used
0
KG Edges Generated
0
Citations Produced
5

Cost Ratios

Cost per KG Edge
0.00 tokens
Lower is better (baseline: 2000)
Cost per Citation
0.00 tokens
Lower is better (baseline: 1000)
Cost per Score Point
0.00 tokens
Tokens / composite_score

Score Impact

Efficiency Boost to Composite
+0.050
10% weight of efficiency score
Adjusted Composite
0.050

How Economics Pricing Works

Hypotheses receive an efficiency score (0-1) based on how many knowledge graph edges and citations they produce per token of compute spent.

High-efficiency hypotheses (score >= 0.8) get a price premium in the market, pulling their price toward $0.580.

Low-efficiency hypotheses (score < 0.6) receive a discount, pulling their price toward $0.420.

Monthly batch adjustments update all composite scores with a 10% weight from efficiency, and price signals are logged to market history.

Related Hypotheses

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TREM2-Dependent Astrocyte-Microglia Cross-talk in Neuroinflammation
Score: 0.000 | neurodegeneration
TREM2-Mediated Microglial Dysfunction Impairs Synaptic Tau Propagation Blockade
Score: 0.000 | neuroscience
TREM2-Mediated Senescent Microglial Reprogramming of Astrocyte Networks
Score: 0.000 | neurodegeneration

Estimated Development

Estimated Cost
$0
Timeline
0 months

🧪 Falsifiable Predictions

No explicit predictions recorded yet. Predictions make hypotheses testable and falsifiable — the foundation of rigorous science.

Knowledge Subgraph (0 edges)

No knowledge graph edges recorded

3D Protein Structure

🧬 TREM2 — PDB 6YXY Click to expand 3D viewer

Experimental structure from RCSB PDB | Powered by Mol* | Rotate: click+drag | Zoom: scroll | Reset: right-click

Source Analysis

Statistical Fine-Mapping of AD GWAS Loci to Identify Causal Variants

neurodegeneration | 2026-04-16 | completed

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