Membrane-derived cofactors in extracellular vesicles maintain polymorph fidelity and templating competence.
Curated pathway from expert analysis
flowchart TD
A["Target Gene: SNCB"]
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.
No curated PDB or AlphaFold mapping for SNCB yet. Search RCSB →
Median TPM across 13 brain regions for SNCB 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 SNCB.
Run python3 scripts/backfill_hypothesis_depmap.py to populate.
| Prediction | Predicted | Observed | Status | Conf |
|---|---|---|---|---|
| IF CSF-derived extracellular vesicles are enzymatically depleted of gangliosides via neuraminidase treatment (removing terminal sialic acids from GM1, GD1a, GT1b), THEN the templating competence of al | ≥50% reduction in RT-QuIC seeding kinetics (increased lag phase and decreased maximum slope) for alpha-synuclein fibrils incubated with ganglioside-depleted EVs | — no observation — | pending | 0.65 |
| IF synthetic gangliosides (GM1, GD1a at 1:1 ratio) are reconstituted into EVs isolated from GBA1-knockout cells (lacking endogenous ganglioside biosynthesis), THEN the preserved alpha-synuclein fibril | Significantly enhanced ThT fluorescence intensity and reduced caspase-cleaved SNCB fragments on Western blot for fibrils pre-incubated with ganglioside-reconsti | — no observation — | pending | 0.58 |