Bidirectional Mendelian randomization analysis of C1Q and ischemic stroke

Exploratory Score: 0.900 Price: $0.50 Ischemic stroke, Atherosclerosis Human genetic association data Status: proposed

What This Experiment Tests

Exploratory experiment designed to discover new patterns targeting C1Q in Human genetic association data. Primary outcome: Causal association between C1Q and ischemic stroke risk

Description

This genetic epidemiological study employed bidirectional Mendelian randomization (MR) analysis to investigate the causal relationship between C1Q levels and ischemic stroke risk, specifically focusing on large artery atherosclerosis subtype. The analysis used genetic variants associated with C1Q as instrumental variables to assess causality while avoiding confounding factors that typically plague observational studies. Inverse variance weighting (IVW) was employed as the primary statistical method. The bidirectional approach allowed assessment of causality in both directions - whether C1Q influences stroke risk and whether stroke risk influences C1Q levels. This approach leverages the random assortment of genetic variants to provide evidence for causal relationships.

TARGET GENE
MODEL SYSTEM
Human genetic association data
ESTIMATED COST
$0
TIMELINE
0 months
PATHWAY
Complement signaling pathway
SOURCE
extracted_from_pmid_38179058
PRIMARY OUTCOME
Causal association between C1Q and ischemic stroke risk

Scoring Dimensions

Info Gain 0.00 (25%) Feasibility 0.00 (20%) Hyp Coverage 0.00 (20%) Cost Effect. 0.00 (15%) Novelty 0.00 (10%) Ethical Safety 0.00 (10%) 0.900 composite

📖 Wiki Pages

C1QA Gene — Complement Component 1q A ChaingeneC1Q Protein (Complement Component 1q)proteinStrokediseaseStrokedisease

Protocol

Bidirectional Mendelian randomization analysis using IVW as primary method, with C1Q as exposure and ischemic stroke as outcome

Expected Outcomes

Identification of causal relationship between C1Q and stroke risk

Success Criteria

Statistically significant association with appropriate confidence intervals

Related Hypotheses (7)

Astrocyte-Microglia Communication Rebalancing via Cytokine Modulation0.655
TREM2-C1Q Competitive Binding to Prevent Complement-Mediated Cholinergic Synapse Loss0.591
Complement C1q-Mediated Synaptic Pruning Drives Early Cognitive Decline in Alzheimer's Disease0.769
NFκB/C1Q SASP Modulation for Synaptic Protection0.534
Tripartite Synapse Cell Type-Nonautonomous Crosstalk: Coordinated Failure0.510

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