ID: h-a3580b22
Hypothesis

Retromer-dependent retrograde endosomal signaling compartmentalization as biomarker and intervention point

VPS26/VPS29/VPS35 retromer complex maintains axonal endosomal signaling microdomains controlling TrkB/p75NTR trafficking.
🧬 VPS35, VPS26, VPS29 (retromer complex); TrkB/NTRK2 (cargo receptors)🩺 neuroscience🎯 Composite 64%💱 $0.60▼17.4%proposed
EvidencePending (0%)📖 0 cit🗣 1 debates 4 support 2 oppose
✓ All Quality Gates Passed
Mechanistic 0.68 (15%) Evidence 0.62 (15%) Novelty 0.62 (12%) Feasibility 0.55 (12%) Impact 0.65 (12%) Druggability 0.58 (10%) Safety 0.75 (8%) Competition 0.68 (6%) Data Avail. 0.55 (5%) Reproducible 0.60 (5%) KG Connect 0.50 (8%) 0.645 composite

🧪 Overview

VPS26/VPS29/VPS35 retromer complex maintains axonal endosomal signaling microdomains controlling TrkB/p75NTR trafficking. Impaired retromer causes somatodendritic receptor mislocalization disrupting synaptic plasticity. TrkB-mScarlet time-lapse imaging in microfluidic chambers provides compartmentalization index (somatic/axonal fluorescence ratio). CCN1 bicyclic peptide is proof-of-mechanism agonist but requires IND-enabling studies. VPS35 P294S variant increases AD risk; VPS35 mutations linked to late-onset PD.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
    A["VPS35-VPS26-VPS29<br/>Retromer Core Trimer"]
    B["Endosomal Cargo Recognition<br/>CI-MPR/ATG9/SorLA Retrieval"]
    C["Retrograde Trafficking<br/>Endosome-to-TGN"]
    D["WASH Complex Recruitment<br/>Actin Branching on Endosome"]
    E["Cathepsin D Maturation<br/>Lysosomal Hydrolase Sorted"]
    F["VPS35 D620N Mutation<br/>Parkinson's PARK17"]
    G["Lysosomal Dysfunction<br/>Alpha-Synuclein Accumulation"]
    A --> B
    B --> C
    C --> D
    C --> E
    F -.->|"impairs"| A
    F --> G
    style A fill:#1a237e,stroke:#4fc3f7,color:#4fc3f7
    style E fill:#1b5e20,stroke:#81c784,color:#81c784
    style F fill:#b71c1c,stroke:#ef9a9a,color:#ef9a9a
    style G fill:#b71c1c,stroke:#ef9a9a,color:#ef9a9a

⚖️ Evidence

⚖️ Evidence Matrix4 supports2 contradicts
Supports
VPS35 P294S variant increases Alzheimer's disease risk
Supports
VPS35 mutations linked to late-onset Parkinson's disease
Supports
Retrograde axonal transport defects precede motor symptoms in PD models
Supports
Retromer agonism by bicyclic peptide CCN1 enhances neurotrophin signaling
Contradicts
No published lead compounds for retromer enhancement; CCN1 has not entered IND-enabling studies
Contradicts
Retromer enhancement is a maintenance strategy; may not reverse established trafficking defects; therapeutic window likely limited to prodromal disease stages
📖 Linked Papers

No linked papers recorded for this hypothesis yet.

🏥 Translation

🧬 3D Protein Structure — VPS35

No curated PDB or AlphaFold mapping for VPS35 yet. Search RCSB →

🧠 GTEx v10 Brain ExpressionJSON

Median TPM across 13 brain regions for VPS35, VPS26, VPS29 (retromer complex); TrkB/NTRK2 (cargo receptors) from GTEx v10.

Cerebellar Hemisphere34.4 Frontal Cortex BA933.4 Cerebellum26.2 Hypothalamus25.3 Cortex22.4 Spinal cord cervical c-120.6 Anterior cingulate cortex BA2420.6 Nucleus accumbens basal ganglia19.9 Caudate basal ganglia18.0 Substantia nigra16.9 Hippocampus14.7 Amygdala13.7 Putamen basal ganglia13.4median TPM (GTEx v10)

💉 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 VPS35, VPS26, VPS29 (retromer complex); TrkB →

No DepMap CRISPR Chronos data found for VPS35, VPS26, VPS29 (retromer complex); TrkB.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

🏆 Tournament

🏆 Arenas / Elo

No arena matches recorded yet. Browse Arenas →

📊 Market Indicators

7d Trend
Falling
7d Momentum
▼ 1.4%
Volatility
Medium
0.0372
Events (7d)
3
Price History
▼17.4%

💾 Resource Usage

LLM Tokens
13,784
$0.0414
Total Cost
$0.0414

🔮 Predictions

🔎 Predictions vs Observations2 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
IF VPS35 is knocked down in primary rat cortical neurons, THEN the axonal/somatic TrkB‑mScarlet fluorescence ratio will decrease by at least 30% within 48 h after transfection.Axonal/somatic TrkB‑mScarlet fluorescence ratio reduced by ≥30% relative to scrambled‑siRNA control.— no observation —pending0.75
IF CCN1 bicyclic peptide (10 mg/kg, i.p., daily) is administered to VPS35 P294S knock‑in mice for 4 weeks, THEN their Morris water maze escape latency will improve, reflected by a ≥20% reduction in laMorris water maze escape latency reduced by ≥20% in CCN1‑treated versus vehicle‑treated VPS35 P294S mice.— no observation —pending0.70
🔮 Falsifiable Predictions (2)
pendingconf 75%
IF VPS35 is knocked down in primary rat cortical neurons, THEN the axonal/somatic TrkB‑mScarlet fluorescence ratio will decrease by at least 30% within 48 h after transfection.
Predicted outcome: Axonal/somatic TrkB‑mScarlet fluorescence ratio reduced by ≥30% relative to scrambled‑siRNA control.
Falsification: No significant change in fluorescence ratio (<5% difference) following VPS35 knockdown.
pendingconf 70%
IF CCN1 bicyclic peptide (10 mg/kg, i.p., daily) is administered to VPS35 P294S knock‑in mice for 4 weeks, THEN their Morris water maze escape latency will improve, reflected by a ≥20% reduction in latency compared with vehicle‑treated mice within the 4‑week treatment window.
Predicted outcome: Morris water maze escape latency reduced by ≥20% in CCN1‑treated versus vehicle‑treated VPS35 P294S mice.
Falsification: No statistically significant difference in escape latency between CCN1‑treated and vehicle‑treated groups (p > 0.05).
Metadatasource: v1_phase_c_backfill · origin_type: gap_debate
sourcev1_phase_c_backfill
origin_typegap_debate
_schema_version1
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting 0 contradicting 0 neutral
Public annotations (0)Annotate on Hypothes.is →
No public annotations yet.