🧪
hypothesis

Pericyte-First Sequential Biomarker Cascade — Soluble PDGFR-β as Sentinel Event in Pre-Symptomatic AD

Hypothesis

Pericyte-First Sequential Biomarker Cascade — Soluble PDGFR-β as Sentinel Event in Pre-Symptomatic AD

CSF soluble PDGFR-β shedding from pericytes as the earliest detectable molecular event in AD, preceding amyloid/tau pathology and exploitable as a 'zero-stage' biomarker via ADAM10/17-mediated ectodomain shedding.
🧬 PDGFRB🎯 Composite 66%💱 $0.53▼5.7%proposed
neurodegeneration
EvidencePending (0%)📖 5 cit🗣 1 debates 5 support 2 oppose
✓ All Quality Gates Passed
Mechanistic 0.82 (15%) Evidence 0.18 (15%) Novelty 0.76 (12%) Feasibility 0.68 (12%) Impact 0.00 (12%) Druggability 0.42 (10%) Safety 0.48 (8%) Competition 0.65 (6%) Data Avail. 0.80 (5%) Reproducible 0.74 (5%) KG Connect 0.50 (8%) 0.662 composite
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arXiv PreprintNeurIPSNature MethodsPLOS ONE
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Composite66%

🧪 Overview

CSF soluble PDGFR-β shedding from pericytes as the earliest detectable molecular event in AD, preceding amyloid/tau pathology and exploitable as a 'zero-stage' biomarker via ADAM10/17-mediated ectodomain shedding. Biomarker utility is strong; therapeutic translation requires novel PDGFR-β agonism or ADAM10/17-selective CNS inhibition.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
    A["PDGFRB Activation<br/>PDGF-BB Ligand Binding"]
    B["Pericyte Recruitment<br/>Blood-Brain Barrier Maintenance"]
    C["PDGFRB Signaling<br/>PI3K/AKT and MAPK Pathways"]
    D["Pericyte Coverage<br/>Capillary Integrity"]
    E["BBB Integrity Loss<br/>Pericyte Dropout in AD"]
    F["Neurovascular Coupling<br/>Functional Hyperemia Impaired"]
    G["Amyloid Deposition<br/>Cerebral Amyloid Angiopathy"]
    H["Hypoperfusion<br/>Chronic Ischemia"]
    I["Cognitive Decline<br/>Vascular contributions to dementia"]
    A --> B
    B --> C
    C --> D
    D --> E
    E --> F
    F --> H
    E --> G
    G --> H
    H --> I
    style A fill:#1a237e,stroke:#4fc3f7,color:#4fc3f7
    style I fill:#b71c1c,stroke:#ef9a9a,color:#ef9a9a

⚖️ Evidence

⚖️ Evidence Matrix5 supports0 contradicts
Supports
Multi-analyte proteomic analysis identifies blood-based neuroinflammation, cerebrovascular and synaptic biomarkers in preclinical Alzheimer's disease.
Mol Neurodegener2024PMID:39385222medium
Supports
c-KIT inhibitors reduce pathology and improve behavior in the Tg(SwDI) model of Alzheimer's disease.
Life Sci Alliance2024PMID:39009412medium
Supports
Presenilins mediate phosphatidylinositol 3-kinase/AKT and ERK activation via select signaling receptors. Selectivity of PS2 in platelet-derived growth factor signaling.
J Biol Chem2005PMID:16014629medium
Supports
Is later-life depression a risk factor for Alzheimer's disease or a prodromal symptom: a study using post-mortem human brain tissue?
Alzheimers Res Ther2023PMID:37700368medium
Supports
Associations of plasma SMOC1 and soluble IL6RA levels with the progression from mild cognitive impairment to dementia.
Brain Behav Immun Health2024PMID:39640195medium
📖 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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🔮 Predictions

🔎 Predictions vs Observations2 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
IF cognitively normal individuals aged 60-80 with elevated baseline CSF sPDGFR-β (top quartile) are stratified and followed longitudinally for 36 months, THEN they will demonstrate significantly fastesPDGFR-β elevation precedes and predicts accelerated amyloid/tau pathology accumulation over 36 months, with effect size ≥15% difference in biomarker trajectori— no observation —pending0.65
IF human brain pericytes in primary culture are treated with selective ADAM10 (Ro 28-1663) and ADAM17 (TMI-005) inhibitors either individually or in combination (25μM each, 48h), THEN combined ADAM10/sPDGFR-β shedding from pericytes requires coordinated ADAM10 and ADAM17 activity, with ≥60% reduction when both are inhibited simultaneously.— no observation —pending0.45
🔮 Falsifiable Predictions (2)
pendingconf 65%
IF cognitively normal individuals aged 60-80 with elevated baseline CSF sPDGFR-β (top quartile) are stratified and followed longitudinally for 36 months, THEN they will demonstrate significantly faster accumulation of amyloid pathology (≥15% greater decline in CSF Aβ42/40 ratio) and tau pathology (≥
Predicted outcome: sPDGFR-β elevation precedes and predicts accelerated amyloid/tau pathology accumulation over 36 months, with effect size ≥15% difference in biomarker
Falsification: No significant difference in amyloid/tau biomarker change rates between sPDGFR-β quartiles (p>0.05 for group × time interaction), OR sPDGFR-β changes occur after rather than before amyloid/tau changes
pendingconf 45%
IF human brain pericytes in primary culture are treated with selective ADAM10 (Ro 28-1663) and ADAM17 (TMI-005) inhibitors either individually or in combination (25μM each, 48h), THEN combined ADAM10/17 inhibition will reduce secreted sPDGFR-β in conditioned media by ≥60% compared to vehicle control
Predicted outcome: sPDGFR-β shedding from pericytes requires coordinated ADAM10 and ADAM17 activity, with ≥60% reduction when both are inhibited simultaneously.
Falsification: Combined ADAM10/17 inhibition produces <40% reduction in sPDGFR-β (fails to implicate these sheddases); OR single-agent inhibition produces ≥50% reduction (suggesting single sheddase is sufficient, co
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