🧪
hypothesis

CCL2-CCR2 Driven Macrophage Infiltration Selectively Strips Fast-Fatigable NMJs via MMP-9 in ALS

Hypothesis

CCL2-CCR2 Driven Macrophage Infiltration Selectively Strips Fast-Fatigable NMJs via MMP-9 in ALS

CCR2+ monocyte-derived macrophages, recruited to the neuromuscular junction by motor neuron-secreted CCL2, selectively infiltrate and strip fast-fatigable (IIb/IIx fibre) NMJs via matrix metalloproteinase-9 (MMP-9) cleavage of the lamini.
🧬 CCL2🩺 als🎯 Composite 68%💱 $0.52▼0.4%open
neurodegeneration
EvidencePending (0%)📖 5 cit🗣 1 debates 5 support 2 oppose
✓ All Quality Gates Passed
Mechanistic 0.80 (15%) Evidence 0.42 (15%) Novelty 0.78 (12%) Feasibility 0.68 (12%) Impact 0.82 (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%) 0.682 composite
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🧪 Overview

CCR2+ monocyte-derived macrophages, recruited to the neuromuscular junction by motor neuron-secreted CCL2, selectively infiltrate and strip fast-fatigable (IIb/IIx fibre) NMJs via matrix metalloproteinase-9 (MMP-9) cleavage of the laminin alpha-5/beta-2 NMJ scaffold. Fast motor neurons express higher CCL2 and lower TIMP-1 (MMP-9 inhibitor) than slow motor units, creating a chemokine gradient that explains selective NMJ vulnerability. Genetic or pharmacological MMP-9 blockade should preferentially protect fast-fatigable NMJs in ALS mouse models.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
    A["ALS Motor Neuron Stress<br/>Fast-Fatigable Type IIb/IIx Units"]
    B["CCL2 Secreted by Fast Motor Neurons<br/>High CCL2 Low TIMP-1 Gradient"]
    C["CCR2+ Monocyte Recruitment<br/>Chemokine-Directed Infiltration"]
    D["Monocyte-Derived Macrophages<br/>Accumulate at Fast-Fatigable NMJ"]
    E["MMP-9 Secretion<br/>Metalloproteinase Activation"]
    F["Laminin alpha5 beta2 Scaffold Cleaved<br/>NMJ Structural Disruption"]
    G["Fast-Fatigable NMJ Stripped<br/>Selective Denervation"]
    H["ALS Motor Neuron Vulnerability<br/>Progressive Weakness"]
    A --> B
    B --> C
    C --> D
    D --> E
    E --> F
    F --> G
    G --> H
    style B fill:#7b1fa2,stroke:#ce93d8,color:#ce93d8
    style H fill:#b71c1c,stroke:#ef9a9a,color:#ef9a9a

⚖️ Evidence

⚖️ Evidence Matrix5 supports0 contradicts
Supports
MCP1-CCR2 and neuroinflammation in the ALS motor cortex with TDP-43 pathology.
J Neuroinflammation2019PMID:31666087medium
Supports
The CCL2-CCR2 axis drives neuromuscular denervation in amyotrophic lateral sclerosis.
Nat Commun2025PMID:40750607medium
Supports
Vascular endothelial growth factor-A (VEGF-A) and chemokine ligand-2 (CCL2) in amyotrophic lateral sclerosis (ALS) patients.
J Neuroinflammation2011PMID:21569455medium
Supports
CCR2 is localized in microglia and neurons, as well as infiltrating monocytes, in the lumbar spinal cord of ALS mice.
Mol Brain2020PMID:32349774medium
Supports
Possible association between expression of chemokine receptor-2 (CCR2) and amyotrophic lateral sclerosis (ALS) patients of North India.
PLoS One2012PMID:22685564medium
📖 Linked Papers

No linked papers recorded for this hypothesis yet.

🏥 Translation

🧬 3D Protein Structure — CCL2

No curated PDB or AlphaFold mapping for CCL2 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 CCL2 →

No DepMap CRISPR Chronos data found for CCL2.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

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💾 Resource Usage

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