Specific lipoprotein particles bind fibril surfaces and preserve polymorph architecture and seeding fidelity outside the cellular environment.
Curated pathway from expert analysis
flowchart TD
A["Target Gene: APOE"]
B["Molecular Mechanism<br/>Pathway Activation"]
C["Cellular Phenotype<br/>Neuronal / Glial Response"]
D["Network Effect<br/>Circuit-Level Consequence"]
E["Disease Relevance<br/>Neurodegeneration Link"]
A --> B --> C --> D --> E
style A fill:#1a237e,stroke:#4fc3f7,color:#4fc3f7
style E fill:#1b5e20,stroke:#81c784,color:#81c784No linked papers recorded for this hypothesis yet.
Median TPM across 13 brain regions for APOE from GTEx v10.
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.
No DepMap CRISPR Chronos data found for APOE.
Run python3 scripts/backfill_hypothesis_depmap.py to populate.
| Prediction | Predicted | Observed | Status | Conf |
|---|---|---|---|---|
| IF ApoE and clusterin are immunodepleted from Parkinson's disease CSF using anti-ApoE (e.g., HJ6.3) and anti-clusterin (e.g., G7) antibodies, THEN the residual fibril seeding activity measured by real | ≥50% reduction in ThT fluorescence maximum rate (seconds⁻¹) and延长lag phase in RT-QuIC assay using αSyn substrates (recombinant human αSyn 1-140) | — no observation — | pending | 0.65 |
| IF recombinant human ApoE3 (10 μg/mL) and clusterin (50 μg/mL) are added to pre-formed αSyn fibril polymorphs derived from DLB patient brain tissue, THEN the structural integrity of distinct strain co | Proteolysis-resistant peptide fragments will match the initial fibril polymorph signature (≥80% similarity) in lipoprotein-coated samples, whereas uncoated fibr | — no observation — | pending | 0.55 |