🧪
hypothesis

CD38 Inhibition for NAD+ Restoration and Microglial Senescence Prevention

Hypothesis

CD38 Inhibition for NAD+ Restoration and Microglial Senescence Prevention

High risk.
🧬 CD38🩺 neurodegeneration🎯 Composite 57%💱 $0.54▼5.9%proposed
EvidencePending (0%)📖 0 cit🗣 1 debates 4 support 4 oppose
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arXiv PreprintNeurIPSNature MethodsPLOS ONE
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Composite57%

🧪 Overview

High risk. The Expert identifies a fatal flaw: CD38 is predominantly expressed in peripheral immune cells (B cells, T cells, NK cells), not microglia. The cited 3-4 fold increase in PD substantia nigra microglia may reflect perivascular macrophage infiltration rather than intrinsic microglial CD38. Multiple clinical-stage CD38 inhibitors exist (evobrutinib approved for MS), but none are being developed for neurodegeneration. This hypothesis should not proceed without microglial-specific CD38 validation in human PD substantia nigra using single-cell approaches.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
    A["Target Gene: CD38"]
    B["Molecular Mechanism<br/>Pathway Activation"]
    C["Cellular Phenotype<br/>Neuronal or Glial Response"]
    D["Network Effect<br/>Circuit-Level Consequence"]
    E["Disease Relevance<br/>Neurodegeneration Link"]
    A --> B --> C --> D --> E
    style A fill:#1a237e,stroke:#4fc3f7,color:#4fc3f7
    style E fill:#1b5e20,stroke:#81c784,color:#81c784

⚖️ Evidence

⚖️ Evidence Matrix4 supports4 contradicts
Supports
CD38 expression increases 3-4 fold in PD substantia nigra microglia
PMID:29894451
Supports
CD38 knockout mice show improved NAD+ levels and reduced neuroinflammation
PMID:30642922
Supports
Microglial NAD+ decline drives pro-inflammatory reprogramming in aging
PMID:30742095
Supports
Multiple CD38 inhibitors clinically available (evobrutinib approved for MS)
PMID:EMBRACE trial
Contradicts
CD38 is predominantly expressed in peripheral immune cells, not microglia
PMID:Perry lab scRNA-seq datasets
Contradicts
CD38 in neurons functions primarily in calcium signaling, not NAD+ metabolism
PMID:25634420
Contradicts
Direct NAD+ precursor supplementation shows inconsistent CNS effects in human trials
PMID:31079879
Contradicts
Species differences: murine microglia express CD38 at much lower basal levels
PMID:30642922
📖 Linked Papers

No linked papers recorded for this hypothesis yet.

🏥 Translation

🧬 3D Protein Structure — CD38

🧬 PDB 1YH3 Click to expand

Experimental structure from RCSB PDB | Powered by Mol*

🧠 GTEx v10 Brain ExpressionJSON

Median TPM across 13 brain regions for CD38 from GTEx v10.

Caudate basal ganglia7.2 Putamen basal ganglia5.5 Nucleus accumbens basal ganglia5.0 Substantia nigra4.0 Hypothalamus3.6 Hippocampus2.9 Anterior cingulate cortex BA242.8 Frontal Cortex BA92.6 Amygdala2.6 Cortex2.4 Spinal cord cervical c-11.4 Cerebellum0.7 Cerebellar Hemisphere0.5median 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 CD38 →

No DepMap CRISPR Chronos data found for CD38.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

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📊 Market Indicators

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💾 Resource Usage

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🔮 Predictions

🔎 Predictions vs Observations2 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
IF we perform single-cell RNA sequencing (scRNA-seq) of CD45+ immune cells isolated from post-mortem Parkinson's disease substantia nigra tissue AND stratify cells by canonical microglial markers (P2RCD38 expression (log2 normalized counts) will be significantly elevated (p<0.001) in P2RY12-negative perivascular macrophages relative to P2RY12-positive microg— no observation —pending0.65
IF we administer a CNS-penetrant CD38 inhibitor (evobrutinib at 20mg/kg twice daily, blood-brain barrier penetrating formulation) to C57BL/6 mice for 4 weeks following MPTP-induced dopaminergic lesionCD38 inhibitor treatment will show ≤10% change in p21+/Iba1+ microglial density (expected ~15 cells/field in vehicle) and ≤5% change in TH+ neuron count (expect— no observation —pending0.45
🔮 Falsifiable Predictions (2)
pendingconf 65%
IF we perform single-cell RNA sequencing (scRNA-seq) of CD45+ immune cells isolated from post-mortem Parkinson's disease substantia nigra tissue AND stratify cells by canonical microglial markers (P2RY12+, TMEM119+, CD64+) versus perivascular macrophage markers (P2RY12-, CD206+, LYVE1+) versus perip
Predicted outcome: CD38 expression (log2 normalized counts) will be significantly elevated (p<0.001) in P2RY12-negative perivascular macrophages relative to P2RY12-posit
Falsification: If scRNA-seq reveals CD38 expression in microglia (P2RY12+/TMEM119+/CD64+ cells) that is comparable to or exceeds expression in perivascular macrophages (fold-change <1.5), the hypothesis that CD38 is
pendingconf 45%
IF we administer a CNS-penetrant CD38 inhibitor (evobrutinib at 20mg/kg twice daily, blood-brain barrier penetrating formulation) to C57BL/6 mice for 4 weeks following MPTP-induced dopaminergic lesion AND compare outcomes to vehicle-treated controls, THEN we will observe no significant difference in
Predicted outcome: CD38 inhibitor treatment will show ≤10% change in p21+/Iba1+ microglial density (expected ~15 cells/field in vehicle) and ≤5% change in TH+ neuron cou
Falsification: If CD38 inhibitor treatment produces ≥30% reduction in microglial p21+/Iba1+ cell density AND/OR ≥25% increase in TH+ neuron survival compared to vehicle controls, the hypothesis that peripheral CD38
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