🧪
hypothesis

Soluble PDGFRβ as a Peripheral Indicator of Pericyte-Mediated Blood-Brain Barrier Breakdown in Preclinical Neurodegeneration

Hypothesis

Soluble PDGFRβ as a Peripheral Indicator of Pericyte-Mediated Blood-Brain Barrier Breakdown in Preclinical Neurodegeneration

Pericyte loss in Alzheimer's disease leads to proteolytic shedding of PDGFRβ into circulation, providing a blood-accessible marker of pericyte injury.
🧬 PDGFRB (Platelet-Derived Growth Factor Receptor Beta)🎯 Composite 70%💱 $0.56▼15.6%proposed
neurodegeneration
EvidencePending (0%)📖 8 cit🗣 1 debates 8 support 3 oppose
✓ All Quality Gates Passed
Mechanistic 0.80 (15%) Evidence 0.43 (15%) Novelty 0.35 (12%) Feasibility 0.48 (12%) Impact 0.00 (12%) Druggability 0.00 (10%) Safety 0.37 (8%) Competition 0.00 (6%) Data Avail. 0.00 (5%) Reproducible 0.70 (5%) KG Connect 0.50 (8%) 0.705 composite
☰ Compare⚔️ Duel⚛️ Collide
📄 Export LaTeX
arXiv PreprintNeurIPSNature MethodsPLOS ONE
📖 Export BibTeXinteract with this hypothesis
Composite70%

🧪 Overview

Pericyte loss in Alzheimer's disease leads to proteolytic shedding of PDGFRβ into circulation, providing a blood-accessible marker of pericyte injury. Circulating PDGFRβ correlates with BBB permeability and cognitive decline. Critical weakness: PDGFRβ is not pericyte-specific (expressed on vascular smooth muscle cells, fibroblasts, hepatic stellate cells), making source attribution essential before clinical deployment.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
A["Abeta deposition"] --> B["Pericyte injury and loss"]
B --> C["PDGFRbeta proteolytic shedding"]
C --> D["Soluble PDGFRbeta in circulation"]
D --> E["BBB permeability increase"]
E --> F["Neurotoxin extravasation into CNS"]
F --> G["Synapse loss and neuronal dysfunction"]
G --> H["Cognitive decline"]
B --> I["PDGFRbeta polymorphisms increase AD risk"]
J["Therapeutic: PDE3A inhibition"] --> K["Enhanced pericyte survival"]
K --> B
D --> L["Source attribution challenge (VSMC, fibroblasts, hepatic stellate cells)"]
L -.-> H
style A fill:#ef5350,stroke:#c62828,color:#fff
style B fill:#ef5350,stroke:#c62828,color:#fff
style C fill:#4fc3f7,stroke:#0288d1,color:#000
style D fill:#4fc3f7,stroke:#0288d1,color:#000
style E fill:#ef5350,stroke:#c62828,color:#fff
style F fill:#ef5350,stroke:#c62828,color:#fff
style G fill:#ef5350,stroke:#c62828,color:#fff
style H fill:#ffd54f,stroke:#f9a825,color:#000
style I fill:#ef5350,stroke:#c62828,color:#fff
style J fill:#81c784,stroke:#388e3c,color:#000
style K fill:#81c784,stroke:#388e3c,color:#000
style L fill:#ffd54f,stroke:#f9a825,color:#000

⚖️ Evidence

⚖️ Evidence Matrix8 supports3 contradicts
Supports
Pericyte loss precedes neurodegeneration in AD models
PMID:30635418
Supports
Circulating PDGFRβ reflects pericyte coverage in human cohorts
PMID:35803576
Supports
PDGFRβ polymorphisms associated with AD risk
PMID:31829146
Supports
Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders.
Nat Rev Neurosci2011PMID:22048062medium
Supports
The blood-brain barrier in systemic inflammation.
Brain Behav Immun2017PMID:26995317medium
Supports
Role of Blood-Brain Barrier in Alzheimer's Disease.
J Alzheimers Dis2018PMID:29782323medium
Supports
The blood-brain barrier in Alzheimer's disease.
Neurobiol Dis2017PMID:27425887medium
Supports
Blood-Brain Barrier Breakdown in Alzheimer's Disease: Mechanisms and Targeted Strategies.
Int J Mol Sci2023PMID:38003477medium
Contradicts
PDGFRβ+ perivascular fibroblasts distinct from pericytes complicate pericyte-specific attribution
PMID:31320688
Contradicts
Pericyte coverage changes in aging are highly variable and don't always correlate with cognitive outcomes
PMID:unknown
Contradicts
AD risk association was modest (OR ~1.3) and not replicated in independent cohorts
PMID:31829146
📖 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 (Platelet-Derived Growth Factor Receptor Beta) →

No DepMap CRISPR Chronos data found for PDGFRB (Platelet-Derived Growth Factor Receptor Beta).

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
▼ 1.2%
Volatility
Medium
0.0291
Events (7d)
3
Price History
▼15.6%

💾 Resource Usage

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

🔮 Predictions

🔎 Predictions vs Observations1 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
If soluble PDGFRβ in plasma reflects pericyte degeneration, then sPDGFRβ will correlate with the rate of BBB integrity decline (DCE-MRI Ktrans slope) and with cognitive deterioration rate, independentIn a 2-year longitudinal AD cohort (n≥100 with amyloid PET, DCE-MRI, and plasma sPDGFRβ), baseline sPDGFRβ in top tertile predicts accelerated Ktrans decline (>— no observation —pending0.78
🔮 Falsifiable Predictions (1)
pendingconf —
If soluble PDGFRβ in plasma reflects pericyte degeneration, then sPDGFRβ will correlate with the rate of BBB integrity decline (DCE-MRI Ktrans slope) and with cognitive deterioration rate, independent of amyloid plaque burden and brain atrophy.
Predicted outcome: In a 2-year longitudinal AD cohort (n≥100 with amyloid PET, DCE-MRI, and plasma sPDGFRβ), baseline sPDGFRβ in top tertile predicts accelerated Ktrans
Falsification: sPDGFRβ does not predict BBB decline rate or cognitive trajectory after adjustment for amyloid and atrophy; pericyte marker changes are secondary to neurodegeneration markers, not independent drivers.
View on SciDEX ↗