🧪
hypothesis

Elevated Circulating sPDGFRβ Reflects Early Pericyte Loss Preceding Neurodegeneration

Hypothesis

Elevated Circulating sPDGFRβ Reflects Early Pericyte Loss Preceding Neurodegeneration

Pericyte degeneration in neurodegeneration leads to proteolytic shedding of the PDGFRβ ectodomain.
🧬 PDGFRB🎯 Composite 60%💱 $0.61▼4.1%proposed
neurodegeneration
EvidencePending (0%)📖 0 cit🗣 1 debates 3 support 3 oppose
✓ All Quality Gates Passed
Mechanistic 0.64 (15%) Evidence 0.34 (15%) Novelty 0.00 (12%) Feasibility 0.00 (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%) 0.600 composite
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arXiv PreprintNeurIPSNature MethodsPLOS ONE
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Composite60%

🧪 Overview

Pericyte degeneration in neurodegeneration leads to proteolytic shedding of the PDGFRβ ectodomain. Soluble PDGFRβ (sPDGFRβ) enters peripheral circulation and may serve as an early, blood-based biomarker reflecting pericyte coverage decline before significant neuronal loss. However, peripheral sources (vascular smooth muscle, fibroblasts) significantly confound interpretation, limiting specificity for brain pericyte pathology.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
    A["PDGFRB<br/>Pericyte Marker"]
    B["Soluble PDGFRbeta<br/>Circulating Form"]
    C["Pericyte<br/>Damage Signal"]
    D["BBB<br/>Permeabilization"]
    E["Neurovascular<br/>Dysfunction"]
    F["Early Neurodegeneration<br/>Prodromal Signal"]
    G["Biomarker<br/>Blood Panel"]
    A --> B
    B --> C
    C --> D
    D --> E
    E --> F
    A --> G
    F --> G
    style A fill:#1a237e,stroke:#4fc3f7,color:#4fc3f7
    style F fill:#b71c1c,stroke:#ef9a9a,color:#ef9a9a
    style G fill:#1b5e20,stroke:#a5d6a7,color:#a5d6a7

⚖️ Evidence

⚖️ Evidence Matrix3 supports3 contradicts
Supports
Pericyte deficiency in AD mouse models increases BBB breakdown with reduced microvascular coverage
PMID:29415984
Supports
CSF sPDGFRβ elevation correlates with BBB breakdown in human aging and AD, predicting cognitive decline
PMID:25817327
Supports
Pericyte-specific PDGFRβ signaling regulates BBB integrity and Aβ clearance
PMID:30786859
Contradicts
sPDGFRβ elevated in traumatic brain injury independent of pericyte coverage
PMID:31781370
Contradicts
sPDGFRβ elevated in multiple sclerosis without pericyte-specific pathology
PMID:34078534
Contradicts
Peripheral PDGFRβ expression in cardiovascular tissue could confound circulating levels
PMID:34078534
📖 Linked Papers

No linked papers recorded for this hypothesis yet.

🏥 Translation

🧬 3D Protein Structure — PDGFRB

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

💉 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 PDGFRB →

No DepMap CRISPR Chronos data found for PDGFRB.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

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📊 Market Indicators

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💾 Resource Usage

No resource usage or linked notebooks recorded for this hypothesis yet.

🔮 Predictions

🔎 Predictions vs Observations2 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
IF we measure circulating sPDGFRβ via ELISA in early Alzheimer's disease (preclinical/prodromal stages, CDR 0-0.5) compared to age-matched cognitively normal controls, THEN we expect significantly eleElevated plasma sPDGFRβ (≥30% above control mean) in preclinical AD group at baseline, with the elevation preceding measurable NfL/tau increases by ≥12 months— no observation —pending0.52
IF we perform selective brain pericyte ablation using pharmacological PDGFRβ inhibition (imatinib, 50mg/kg/day for 4 weeks) in C57BL/6 mice versus peripheral smooth muscle cell injury (wire injury to Brain-specific pericyte injury model: sPDGFRβ elevated ≥40% vs. vehicle, brain NG2+ pericytes reduced ≥30% by IHC; Peripheral injury model: no significant chang— no observation —pending0.48
🔮 Falsifiable Predictions (2)
pendingconf 52%
IF we measure circulating sPDGFRβ via ELISA in early Alzheimer's disease (preclinical/prodromal stages, CDR 0-0.5) compared to age-matched cognitively normal controls, THEN we expect significantly elevated sPDGFRβ levels (≥30% increase, p<0.05) in the AD group reflecting early pericyte loss, BEFORE
Predicted outcome: Elevated plasma sPDGFRβ (≥30% above control mean) in preclinical AD group at baseline, with the elevation preceding measurable NfL/tau increases by ≥1
Falsification: No significant difference in sPDGFRβ between groups, or sPDGFRβ elevation correlating positively only with established neurodegeneration markers (NfL, tau) rather than preceding them, or higher sPDGFR
pendingconf 48%
IF we perform selective brain pericyte ablation using pharmacological PDGFRβ inhibition (imatinib, 50mg/kg/day for 4 weeks) in C57BL/6 mice versus peripheral smooth muscle cell injury (wire injury to femoral artery) without CNS involvement, THEN brain pericyte ablation should produce elevated plasma
Predicted outcome: Brain-specific pericyte injury model: sPDGFRβ elevated ≥40% vs. vehicle, brain NG2+ pericytes reduced ≥30% by IHC; Peripheral injury model: no signifi
Falsification: Peripheral smooth muscle injury produces equivalent or greater sPDGFRβ elevation compared to brain pericyte ablation, indicating systemic sources confound brain-specific detection; OR brain pericyte a
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