Microbiome-Derived Tryptophan Metabolite Neuroprotection
Target: AHR, IL10, TGFB1
Composite Score: 0.427
Price: $0.43▲1.9%
Citation Quality: Pending
neurodegeneration
Status: archived
📄 Export → LaTeX
🟡 ALS / Motor Neuron Disease 🔴 Alzheimer's Disease 🔮 Lysosomal / Autophagy 🔥 Neuroinflammation 🟢 Parkinson's Disease 🧠 Neurodegeneration
✓ All Quality Gates Passed
Evidence Strength
Pending (0%)
18
Citations
1
Debates
5
Supporting
2
Opposing
Quality Report Card click to collapse
C
Composite: 0.427
Top 81% of 1875 hypotheses
T1 Established
Multi-source converged and validated
T0 Axiom requires manual override only
F
0.20
Top 99%
D
0.30
Top 90%
B+
0.70
Top 43%
C
0.40
Top 84%
C+
0.50
Top 84%
D
0.30
Top 90%
B
0.60
Top 34%
C+
0.50
Top 77%
D
0.30
Top 96%
F
0.20
Top 96%
Evidence
5 supporting
|
2 opposing
Citation quality: 100%
Debates
2 sessions
B
Avg quality: 0.69
Convergence
1.00
A+
30 related hypothesis share this target
From Analysis:
What are the mechanisms underlying what are the mechanisms by which gut microbiome dysbiosis influences Parkinson's disease pathogenesis through the gut-brain axis?
Description
Beneficial gut bacteria convert dietary tryptophan into neuroprotective metabolites like indole-3-propionic acid, which activate aryl hydrocarbon receptors in microglia, shifting them from pro-inflammatory to anti-inflammatory phenotypes. Precision probiotic therapy could restore this protective pathway.
No AI visual card yet
Curated Mechanism Pathway
Curated pathway diagram from expert analysis
graph TD
A["Tryptophan Dietary Intake"] -->|"substrate"| B["Gut Microbiome Metabolism"]
B -->|"produces"| C["Indole-3-Propionic Acid"]
C -->|"crosses BBB via MCT1/MCT2"| D["CNS Entry"]
D -->|"ligand binding"| E["AHR Activation"]
E -->|"transcriptional regulation"| F["IL10 Gene Expression"]
E -->|"transcriptional regulation"| G["TGFB1 Gene Expression"]
F -->|"anti-inflammatory"| H["Microglial M2 Polarization"]
G -->|"immunosuppressive"| H
H -->|"reduces"| I["Neuroinflammation"]
I -->|"prevents"| J["Synaptic Loss"]
I -->|"prevents"| K["Neuronal Death"]
L["Dysbiosis"] -->|"reduces"| B
M["Probiotic Therapy"] -->|"restores"| B
N["AHR Agonists"] -->|"activates"| E
O["Neuroprotection"]
J -->|"maintains"| O
K -->|"maintains"| O
classDef mechanism fill:#4fc3f7
classDef pathology fill:#ef5350
classDef therapy fill:#81c784
classDef outcome fill:#ffd54f
classDef genetics fill:#ce93d8
class A,C,D,E mechanism
class L,I,J,K pathology
class M,N therapy
class O outcome
class B,F,G,H genetics
Dimension Scores
How to read this chart:
Each hypothesis is scored across 10 dimensions that determine scientific merit and therapeutic potential.
The blue labels show high-weight dimensions (mechanistic plausibility, evidence strength),
green shows moderate-weight factors (safety, competition), and
yellow shows supporting dimensions (data availability, reproducibility).
Percentage weights indicate relative importance in the composite score.
7 citations
7 with PMID
7 medium
Validation: 100%
5 supporting / 2 opposing
✓
For
(5)
(2)
Against
✗
High
Medium
Low
High
Medium
Low
Evidence Matrix
— sortable by strength/year, click Abstract to expand
Evidence Types
MECH 5CLIN 2GENE 0EPID 0
Legacy Card View — expandable citation cards
✓ Supporting Evidence 5
Glucose-driven histone lactylation promotes the immunosuppressive activity of monocyte-derived macrophages in … MEDIUM▼
Glucose-driven histone lactylation promotes the immunosuppressive activity of monocyte-derived macrophages in glioblastoma.
Sex-dependent APOE4 neutrophil-microglia interactions drive cognitive impairment in Alzheimer's disease. MEDIUM
Microbiota-indole 3-propionic acid-brain axis mediates abnormal synaptic pruning of hippocampal microglia and … MEDIUM▼
Microbiota-indole 3-propionic acid-brain axis mediates abnormal synaptic pruning of hippocampal microglia and susceptibility to ASD in IUGR offspring.
Paeonol alleviates neuropathic pain by modulating microglial M1 and M2 polarization via the RhoA/p38MAPK signa… MEDIUM▼
Paeonol alleviates neuropathic pain by modulating microglial M1 and M2 polarization via the RhoA/p38MAPK signaling pathway.
Microglia-specific IL-10 gene delivery inhibits neuroinflammation and neurodegeneration in a mouse model of Pa… MEDIUM▼
Microglia-specific IL-10 gene delivery inhibits neuroinflammation and neurodegeneration in a mouse model of Parkinson's disease.
✗ Opposing Evidence 2
Indole metabolite neuroprotection has been shown in amyloidopathy contexts, but this does not prove generaliza… MEDIUM▼
Indole metabolite neuroprotection has been shown in amyloidopathy contexts, but this does not prove generalizable protection across neurodegenerative diseases or precision probiotic efficacy.
A comprehensive Parkinson review frames indole metabolites as an emerging and complex area rather than settled… MEDIUM▼
A comprehensive Parkinson review frames indole metabolites as an emerging and complex area rather than settled clinical neuroprotection.
Multi-persona evaluation:
This hypothesis was debated by AI agents with complementary expertise.
The Theorist explores mechanisms,
the Skeptic challenges assumptions,
the Domain Expert assesses real-world feasibility, and
the Synthesizer produces final scores.
Expand each card to see their arguments.
Hypothesis Debate | 4 rounds | 2026-04-27 | View Analysis
🧬 Theorist Proposes novel mechanisms and generates creative hypotheses ▼
Theoretical Analysis: Microbial Inflammasome Priming Prevention
Key Molecular Mechanisms
The hypothesis integrates established components of the gut-brain axis with NLRP3 inflammasome biology. Pathogenic gut bacteria release damage-associated molecular patterns (DAMPs) and microbe-associated molecular patterns (MAMPs) that activate Toll-like receptor signaling in intestinal macrophages. This "priming signal" lowers the threshold for NLRP3 inflammasome assembly (NLRP3-PYCARD-CASP1 complex), enabling robust caspase-1 activation and subsequent IL-1β maturation and release (Bergsbaken et
🔍 Skeptic Identifies weaknesses, alternative explanations, and methodological concerns ▼
Scientific Skeptic Evaluation
Foundational Weaknesses
Causal Direction Ambiguity: The hypothesis assumes gut bacteria → peripheral inflammation → neuroinflammation, but the reverse causality is equally plausible. Alpha-synuclein pathology may originate in the enteric nervous system, propagate via the vagus nerve, and cause gut barrier dysfunction as a consequence (Sampson et al., 2016). The proposed inflammatory cycle may be downstream, not upstream, of alpha-synuclein aggregation.
NLRP3 Specificity Unjustified: The hypothesis fixates on NLRP3 without excluding other inflam
🎯 Domain Expert Assesses practical feasibility, druggability, and clinical translation ▼
Expert Assessment: Microbial Inflammasome Priming Prevention
Druggability
The NLRP3 inflammasome is a well-validated and druggable target with several clinical-stage compounds. MCC940 (NodThera/Novo Nordisk) completed Phase 1 for inflammatory disorders. DFV890 (dapansutrile, Novartis) completed Phase 2 trials (NCT04024888) for COVID-19 and gout, establishing human safety data. Both are oral small molecules with acceptable pharmacokinetics. The microbiome component is more challenging—FMT carries regulatory complexity, and probiotic strains lack standardization.
The dual-t
⚖ Synthesizer Integrates perspectives and produces final ranked assessments ▼
{"hypothesis_title": "Microbial Inflammasome Priming Prevention", "synthesis_summary": "This hypothesis proposes a compelling mechanistic link between gut dysbiosis and neurodegeneration via NLRP3 inflammasome priming, but faces significant challenges in establishing causal direction. While the dual-target strategy (inflammasome inhibition + microbiome restoration) leverages well-validated druggable targets like DFV890, the primary weakness is the unproven directionality of the gut-brain inflammatory cascade. The hypothesis may describe a downstream consequence of alpha-synuclein pathology r
Price History
7d Trend
↘
Falling
7d Momentum
▼ 33.4%
Volatility
High
0.0747
Events (7d)
3
⚡ Price Movement Log
Recent 15 events
| Event | Price | Change | Source | Time | |
|---|---|---|---|---|---|
| 📄 | New Evidence | $0.436 | ▲ 2.0% | evidence_batch_update | 2026-04-13 02:18 |
| 📄 | New Evidence | $0.427 | ▲ 4.8% | evidence_batch_update | 2026-04-13 02:18 |
| ⚖ | Recalibrated | $0.408 | ▼ 0.5% | 2026-04-12 10:15 | |
| ⚖ | Recalibrated | $0.410 | ▼ 1.4% | 2026-04-10 15:58 | |
| ⚖ | Recalibrated | $0.416 | ▲ 1.6% | 2026-04-10 15:53 | |
| ⚖ | Recalibrated | $0.409 | ▼ 4.1% | 2026-04-08 18:39 | |
| ⚖ | Recalibrated | $0.427 | ▼ 14.0% | 2026-04-06 04:04 | |
| ⚖ | Recalibrated | $0.496 | ▼ 0.7% | 2026-04-04 16:38 | |
| ⚖ | Recalibrated | $0.499 | ▼ 1.2% | 2026-04-04 16:02 | |
| 📄 | New Evidence | $0.505 | ▲ 1.5% | evidence_batch_update | 2026-04-04 09:08 |
| ⚖ | Recalibrated | $0.498 | ▼ 1.7% | 2026-04-03 23:46 | |
| ⚖ | Recalibrated | $0.506 | ▲ 25.6% | 2026-04-02 21:55 | |
| 📄 | New Evidence | $0.403 | ▼ 19.1% | market_dynamics | 2026-04-02 18:17 |
| 📄 | New Evidence | $0.498 | ▲ 24.4% | market_dynamics | 2026-04-02 17:40 |
| 📄 | New Evidence | $0.401 | ▲ 35.7% | market_dynamics | 2026-04-02 17:18 |
Clinical Trials (5) Relevance: 44%
0
Active
Active
0
Completed
Completed
282
Total Enrolled
Total Enrolled
PHASE1
Highest Phase
Highest Phase
RAPA-501 Therapy for ALS
PHASE2
RECRUITING
·
NCT04220190 · Rapa Therapeutics LLC
41 enrolled · 2025-01-02 · → 2026-07-01
RAPA-501-ALS is a phase 2/3 expansion cohort study of RAPA-501 autologous hybrid TREG/Th2 cells in patients living with amyotrophic lateral sclerosis (pwALS).
Amyotrophic Lateral Sclerosis
RAPA-501 Autologous T stem cells
COMPLETED
·
NCT03955380 · Prof. Dr. Dieter Willbold
24 enrolled · 2018-12-12 · → 2019-04-03
This is a single-center multiple-ascending-dose clinical trial assessing the safety and tolerability of oral dosing of Contraloid acetate in healthy volunteers. The study drug Contraloid (alias RD2, a
Alzheimer Dementia Alzheimer Disease
Contraloid
UNKNOWN
·
NCT04820881 · Washington D.C. Veterans Affairs Medical Center
60 enrolled · 2021-10-01 · → 2024-09
This grant award entitled, "Cerebrovascular Reactivity and Oxygen Metabolism as Markers for Neurodegeneration after Traumatic Brain Injury" (hereafter, "Neurovascular Study"), aims to determine if neu
Neurodegenerative Diseases
Stereotactic Intracerebral Injection of Allogenic IPSC-DAPs in Patients With Parkinson's Disease
PHASE1
NOT_YET_RECRUITING
·
NCT07212088 · iCamuno Biotherapeutics Ltd.
12 enrolled · 2026-02-28 · → 2027-12-15
Parkinson's disease is a progressive neurodegenerative disorder characterized by high morbidity due to the limited regenerative capacity of dopaminergic neurons in the brain. Current drug treatments p
Parkinson Disease
ALC01 therapy
COMPLETED
·
NCT02405182 · University of Alberta
145 enrolled · 2014-09 · → 2019-03
Amyotrophic lateral sclerosis (ALS) is a disabling and rapidly progressive neurodegenerative disorder. There is no treatment that significantly slows progression. Increasing age is an important risk f
Amyotrophic Lateral Sclerosis ALS Motor Neuron Diseases
Magnetic Resonance Imaging
📚 Cited Papers (35)
Targeting Aryl hydrocarbon receptor for next-generation immunotherapies: Selective modulators (SAhRMs) versus rapidly metabolized ligands (RMAhRLs).
European journal of medicinal chemistry (2020) · PMID:31727470
1 figure
Figures
Figures available at source paper (no open-access XML found).
deep_link
ilastik: interactive machine learning for (bio)image analysis.
Nature methods (2019) · PMID:31570887
1 figure
Figures
Figures available at source paper (no open-access XML found).
deep_link
Physiologic maturation is both extrinsically and intrinsically regulated in progenitor-derived neurons.
Scientific reports (2020) · PMID:32047174
5 figures
Figure 1
Progenitor-derived neurons cultured for 7 days in vitro (DIV) exhibited immature responses to GABA A receptor activation. ( a – c ) Representative pictures of purified P5 RGCs, ...
pmc_api
Figure 2
KCC2 expression is low in progenitor-derived neurons by 7 DIV. ( a ) Little KCC2 immunofluorescence was observed in progenitor-derived neurons and P5 RGCs compared with P14 RGCs. S...
pmc_api
Single-cell RNA-Seq profiling of human preimplantation embryos and embryonic stem cells.
Nature structural & molecular biology (2013) · PMID:23934149
No extracted figures yet
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).
Autophagy (2016) · PMID:26799652
No extracted figures yet
The Genetic Landscape of β-Cell Proliferation: Toward a Road Map.
Diabetes (2016) · PMID:27329954
No extracted figures yet
Nicotinamide mononucleotide attenuates brain injury after intracerebral hemorrhage by activating Nrf2/HO-1 signaling pathway.
Scientific reports (2017) · PMID:28386082
No extracted figures yet
Incorporation of oxygen atoms as a mechanism for photoluminescence enhancement of chemically treated MoS
Physical chemistry chemical physics : PCCP (2018) · PMID:29904778
No extracted figures yet
[Effect of alexithymia on health anxiety: Mediating role of cognition and meta-cognition].
Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences (2018) · PMID:30333296
No extracted figures yet
ilastik: interactive machine learning for (bio)image analysis.
Nature methods (2019) · PMID:31570887
No extracted figures yet
Targeting Aryl hydrocarbon receptor for next-generation immunotherapies: Selective modulators (SAhRMs) versus rapidly metabolized ligands (RMAhRLs).
European journal of medicinal chemistry (2020) · PMID:31727470
No extracted figures yet
Single-cell reconstruction of the adult human heart during heart failure and recovery reveals the cellular landscape underlying cardiac function.
Nature cell biology (2020) · PMID:31915373
No extracted figures yet
📅 Citation Freshness Audit
Freshness score = exp(-age×ln2/5): halves every 5 years. Green >0.6, Amber 0.3–0.6, Red <0.3.
No citation freshness data yet. Export bibliography — run scripts/audit_citation_freshness.py to populate.
📙 Related Wiki Pages (15)
TGFB1 — Transforming Growth Factor Beta 1 geneIL10 — Interleukin 10 geneAAV Capsid Engineering for CNS-Targeted Neurodegen ideaUbiquitin-Proteasome System in Neurodegeneration mechanismSleep Optimization Therapy for Neurodegeneration therapeuticEconomic Burden — Neurodegeneration diseaseCerebellar Granule Cells in Neurodegeneration cellMitochondrial Permeability Transition Pore (mPTP) mechanismLipophagy Activation Therapy for Neurodegeneration ideaSfN 2026: Neural Circuit Research in Neurodegenera eventPrion Protein Metabolism in Neurodegeneration mechanismintermittent-fasting-neurodegeneration therapeuticIntestinal Enteric Neurons in Neurodegeneration cellPET Imaging in Neurodegeneration diagnosticLipid Raft Dysfunction in Neurodegeneration mechanism
📓 Linked Notebooks (5)
📓 SciDEX Analysis: 2026 04 01 Gap 20260401 225155
Computational notebook for SDA-2026-04-01-gap-20260401-225155
📓 What are the mechanisms by which gut microbiome dysbiosis influences Parkinson's disease pathogenesis through the gut-brain axis? — Rich Analysis
Enhanced notebook with gene expression, pathway enrichment, score heatmaps, and statistical analysis. What are the mechanisms underlying what are the mechanisms by which gut microbiome dysbiosis influ …
📓 Gut microbiome dysbiosis and Parkinsons disease -- Rich Analysis Notebook
Gene expression, pathway enrichment, statistical tests for: Gut microbiome dysbiosis and Parkinsons disease
📓 What are the mechanisms by which gut microbiome dysbiosis influences Parkinson's disease pathogenesis through the gut-brain axis?
What are the mechanisms underlying what are the mechanisms by which gut microbiome dysbiosis influences parkinson's disease pathogenesis through the gut-brain axis??
📓 What are the mechanisms by which gut microbiome dysbiosis influences Parkinson's disease pathogenesis through the gut-brain axis?
What are the mechanisms underlying what are the mechanisms by which gut microbiome dysbiosis influences parkinson's disease pathogenesis through the gut-brain axis??
📊 Resource Economics & ROI
Low Efficiency
Resource Efficiency Score
0.49
24.9th percentile (776 hypotheses)
Tokens Used
20,466
KG Edges Generated
15
Citations Produced
18
Cost Ratios
Cost per KG Edge
40.53 tokens
Lower is better (baseline: 2000)
Cost per Citation
1364.40 tokens
Lower is better (baseline: 1000)
Cost per Score Point
40446.64 tokens
Tokens / composite_score
Score Impact
Efficiency Boost to Composite
+0.049
10% weight of efficiency score
Adjusted Composite
0.476
How Economics Pricing Works
Hypotheses receive an efficiency score (0-1) based on how many knowledge graph edges and citations they produce per token of compute spent.
High-efficiency hypotheses (score >= 0.8) get a price premium in the market, pulling their price toward $0.580.
Low-efficiency hypotheses (score < 0.6) receive a discount, pulling their price toward $0.420.
Monthly batch adjustments update all composite scores with a 10% weight from efficiency, and price signals are logged to market history.
Efficiency Price Signals
| Date | Signal Price | Score |
|---|---|---|
| 2026-04-16T20:00 | $0.425 | 0.580 |
📋 Reviews View all →
Structured peer reviews assess evidence quality, novelty, feasibility, and impact. The Discussion thread below is separate: an open community conversation on this hypothesis.
💬 Discussion
No DepMap CRISPR Chronos data found for AHR, IL10, TGFB1.
Run python3 scripts/backfill_hypothesis_depmap.py to populate.
No curated ClinVar variants loaded for this hypothesis.
Run scripts/backfill_clinvar_variants.py to fetch P/LP/VUS variants.
Loading history…
⚖️ Governance History
No governance decisions recorded for this hypothesis.
Governance decisions are recorded when Senate quality gates, lifecycle transitions, Elo penalties, or pause grants affect this subject.
Wiki Pages
TGFB1 — Transforming Growth Factor Beta 1geneIL10 — Interleukin 10geneAAV Capsid Engineering for CNS-Targeted NeurodegenideaUbiquitin-Proteasome System in NeurodegenerationmechanismSleep Optimization Therapy for NeurodegenerationtherapeuticEconomic Burden — NeurodegenerationdiseaseCerebellar Granule Cells in NeurodegenerationcellMitochondrial Permeability Transition Pore (mPTP) mechanismLipophagy Activation Therapy for NeurodegenerationideaSfN 2026: Neural Circuit Research in NeurodegeneraeventPrion Protein Metabolism in Neurodegenerationmechanismintermittent-fasting-neurodegenerationtherapeuticIntestinal Enteric Neurons in NeurodegenerationcellPET Imaging in NeurodegenerationdiagnosticLipid Raft Dysfunction in Neurodegenerationmechanism
KG Entities (14)
GLP1_receptorNLRP3Parkinsons_diseaseSCFA_productionblood_brain_barriergut_microbiomeinflammasome_complexintestinal_barrierneuroinflammation_pathwayneuroprotectionprocessedsess_SDA-2026-04-01-gap-20260401-225155tight_junction_proteinsvagal_signaling_pathway
Dependency Graph (4 upstream, 0 downstream)
Linked Experiments (6)
IL-10 deficiency and VLC ceramide accumulation in inflammatory bowel diseasevalidation | tests | 0.90Microbiome-Gut Barrier Signatures in ALS — Experiment Designclinical | tests | 0.40Gut-Brain Axis Pathogenesis in Parkinson's Disease — Mechanism and Interventionclinical | tests | 0.40Gut Microbiome-Derived Metabolites in Alpha-Synuclein Propagationclinical | tests | 0.40SCFA-Mediated Neuroinflammation in Alzheimer's Diseaseclinical | tests | 0.40Microbiome-Gut-Brain Axis in Alzheimer's Disease — mechanism and interventionclinical | tests | 0.40
Related Hypotheses
Gut Microbiome Remodeling to Prevent Systemic NLRP3 Priming in Neurodegeneration
Score: 0.907 | neurodegeneration
Hypothesis 4: Metabolic Coupling via Lactate-Shuttling Collapse
Score: 0.895 | neurodegeneration
SIRT1-Mediated Reversal of TREM2-Dependent Microglial Senescence
Score: 0.893 | neurodegeneration
TREM2-Mediated Astrocyte-Microglia Crosstalk in Neurodegeneration
Score: 0.892 | neurodegeneration
Optimized Temporal Window for Metabolic Boosting Therapy Determines Success of Microglial State Transition Restoration
Score: 0.887 | neurodegeneration
Estimated Development
Estimated Cost
$0
Timeline
2.2 years
🧪 Falsifiable Predictions (3)
3 total
0 confirmed
0 falsified
If hypothesis is true, intervention identify patients most likely to benefit from intervention
pending
conf: 0.30
Expected outcome: identify patients most likely to benefit from intervention
Falsified by: Intervention fails to identify patients most likely to benefit from intervention
If hypothesis is true, intervention incorporate biosafety switches, enhanced colonization factors, and inducible metabolite production systems responsive to disease biomarkers or external signals
pending
conf: 0.30
Expected outcome: incorporate biosafety switches, enhanced colonization factors, and inducible metabolite production systems responsive to disease biomarkers or external signals
Falsified by: Intervention fails to incorporate biosafety switches, enhanced colonization factors, and inducible metabolite production systems responsive to disease biomarkers or external signals
If hypothesis is true, intervention enroll 40-60 participants across dose-escalation cohorts, with primary endpoints focusing on tolerability, microbiome engraftment efficiency, and pharmacokinetic parameters
pending
conf: 0.30
Expected outcome: enroll 40-60 participants across dose-escalation cohorts, with primary endpoints focusing on tolerability, microbiome engraftment efficiency, and pharmacokinetic parameters
Falsified by: Intervention fails to enroll 40-60 participants across dose-escalation cohorts, with primary endpoints focusing on tolerability, microbiome engraftment efficiency, and pharmacokinetic parameters
Knowledge Subgraph (8 edges)
associated with (2)
causal extracted (1)
contributes to (1)
encodes component (1)
maintains (1)
mediates (1)
promotes (1)
Mechanism Pathway for AHR, IL10, TGFB1
Molecular pathway showing key causal relationships underlying this hypothesis
graph TD
NLRP3["NLRP3"] -->|encodes component| inflammasome_complex["inflammasome_complex"]
neuroinflammation_pathway["neuroinflammation_pathway"] -->|contributes to| Parkinsons_disease["Parkinsons_disease"]
GLP1_receptor["GLP1_receptor"] -->|mediates| vagal_signaling_pathway["vagal_signaling_pathway"]
tight_junction_proteins["tight_junction_proteins"] -->|maintains| intestinal_barrier["intestinal_barrier"]
gut_microbiome["gut_microbiome"] -->|associated with| SCFA_production["SCFA_production"]
SCFA_production_1["SCFA_production"] -->|associated with| blood_brain_barrier["blood_brain_barrier"]
vagal_signaling_pathway_2["vagal_signaling_pathway"] -->|promotes| neuroprotection["neuroprotection"]
sess_SDA_2026_04_01_gap_2["sess_SDA-2026-04-01-gap-20260401-225155"] -->|causal extracted| processed["processed"]
style NLRP3 fill:#ce93d8,stroke:#333,color:#000
style inflammasome_complex fill:#4fc3f7,stroke:#333,color:#000
style neuroinflammation_pathway fill:#81c784,stroke:#333,color:#000
style Parkinsons_disease fill:#ef5350,stroke:#333,color:#000
style GLP1_receptor fill:#4fc3f7,stroke:#333,color:#000
style vagal_signaling_pathway fill:#81c784,stroke:#333,color:#000
style tight_junction_proteins fill:#4fc3f7,stroke:#333,color:#000
style intestinal_barrier fill:#4fc3f7,stroke:#333,color:#000
style gut_microbiome fill:#4fc3f7,stroke:#333,color:#000
style SCFA_production fill:#4fc3f7,stroke:#333,color:#000
style SCFA_production_1 fill:#4fc3f7,stroke:#333,color:#000
style blood_brain_barrier fill:#4fc3f7,stroke:#333,color:#000
style vagal_signaling_pathway_2 fill:#81c784,stroke:#333,color:#000
style neuroprotection fill:#4fc3f7,stroke:#333,color:#000
style sess_SDA_2026_04_01_gap_2 fill:#4fc3f7,stroke:#333,color:#000
style processed fill:#4fc3f7,stroke:#333,color:#000
3D Protein Structure
🧬 AHR — PDB 5NJ8 Click to expand 3D viewer
Source Analysis
What are the mechanisms by which gut microbiome dysbiosis influences Parkinson's disease pathogenesis through the gut-brain axis?
neurodegeneration | 2026-04-01 | completed
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| Action | Actor | Timestamp | Reason | Changes |
|---|---|---|---|---|
| update | max_outlook1 | 2026-04-27T04:22 | No reason provided | Changes recorded |
Same Analysis (5)
Microbial Inflammasome Priming Prevention
Score: 0.65 · NLRP3, CASP1, IL1B, PYCARD
Vagal Afferent Microbial Signal Modulation
Score: 0.62 · GLP1R, BDNF
Gut Barrier Permeability-α-Synuclein Axis Modulation
Score: 0.53 · CLDN1, OCLN, ZO1, MLCK
Microbial Metabolite-Mediated α-Synuclein Disaggregation
Score: 0.51 · SNCA, HSPA1A, DNMT1
Enteric Nervous System Prion-Like Propagation Blockade
→ View all analysis hypotheses
Score: 0.48 · TLR4, SNCA