Bacterial Enzyme-Mediated Dopamine Precursor Synthesis
Target: TH, AADC
Composite Score: 0.384
Price: $0.41▲9.8%
Citation Quality: Pending
neurodegeneration
Status: archived
📄 Export → LaTeX
✓ All Quality Gates Passed
Evidence Strength
Pending (0%)
23
Citations
1
Debates
5
Supporting
2
Opposing
Quality Report Card click to collapse
D
Composite: 0.384
Top 83% of 1875 hypotheses
T5 Contested
Contradicted by evidence, under dispute
D
0.30
Top 97%
F
0.20
Top 97%
A+
0.90
Top 18%
F
0.10
Top 100%
C
0.40
Top 94%
F
0.20
Top 96%
F
0.20
Top 97%
D
0.30
Top 97%
F
0.20
Top 98%
F
0.10
Top 98%
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
Engineered probiotic bacteria expressing tyrosine hydroxylase and aromatic L-amino acid decarboxylase could produce L-DOPA locally in the gut, providing sustained dopamine precursor delivery while bypassing hepatic metabolism and reducing motor fluctuations.
No AI visual card yet
Curated Mechanism Pathway
Curated pathway diagram from expert analysis
graph TD
A["L-Tyrosine
Substrate"] --> B["Tyrosine Hydroxylase
(TH)"]
C["Tetrahydrobiopterin
(BH4)"] --> B
D["O2 and Fe2+
Cofactors"] --> B
B --> E["L-DOPA
Intermediate"]
E --> F["Aromatic L-amino acid
Decarboxylase (AADC)"]
G["Pyridoxal 5'-phosphate
(PLP)"] --> F
F --> H["Dopamine
Product"]
I["GTP Cyclohydrolase I
(GTPCH1)"] --> J["BH4 Biosynthesis
Pathway"]
K["6-pyruvoyl-tetrahydropterin
Synthase (PTPS)"] --> J
J --> C
L["Engineered Probiotic
Bacteria"] --> B
L --> F
L --> I
L --> K
H --> M["Striatal Dopamine
Restoration"]
M --> N["Improved Motor
Function"]
O["Neurodegeneration
Process"] --> P["Dopamine Depletion"]
P --> Q["Motor Dysfunction
Symptoms"]
classDef normal fill:#4fc3f7
classDef therapeutic fill:#81c784
classDef pathology fill:#ef5350
classDef outcome fill:#ffd54f
classDef molecular fill:#ce93d8
class A,C,D,G normal
class B,F,I,J,K,L therapeutic
class O,P,Q pathology
class M,N outcome
class E,H molecular
GTEx v10 Brain Expression
JSONMedian TPM across 13 brain regions for TH, AADC from GTEx v10.
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 3CLIN 3GENE 1EPID 0
Legacy Card View — expandable citation cards
✓ Supporting Evidence 5
Mild/moderate phenotypes in AADC deficiency: Focus on the aromatic amino acid decarboxylase protein. MEDIUM
Compound Heterozygosis in AADC Deficiency and Its Complex Phenotype in Terms of AADC Protein Population. MEDIUM
Gene therapy for aromatic L-amino acid decarboxylase deficiency by MR-guided direct delivery of AAV2-AADC to m… MEDIUM▼
Gene therapy for aromatic L-amino acid decarboxylase deficiency by MR-guided direct delivery of AAV2-AADC to midbrain dopaminergic neurons.
A review of aromatic l-amino acid decarboxylase (AADC) deficiency in Taiwan. MEDIUM
Blood, urine and cerebrospinal fluid analysis in TH and AADC deficiency and the effect of treatment. MEDIUM
✗ Opposing Evidence 2
Gut bacteria can metabolize levodopa through an interspecies pathway, implying engineered gut catecholamine pr… MEDIUM▼
Gut bacteria can metabolize levodopa through an interspecies pathway, implying engineered gut catecholamine precursor production may be degraded or pharmacokinetically unstable.
Gut bacterial tyrosine decarboxylases restrict levodopa levels, directly challenging assumptions that intestin… MEDIUM▼
Gut bacterial tyrosine decarboxylases restrict levodopa levels, directly challenging assumptions that intestinal bacterial dopamine-precursor handling is reliably beneficial.
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
▼ 37.4%
Volatility
High
0.0870
Events (7d)
4
⚡ Price Movement Log
Recent 15 events
| Event | Price | Change | Source | Time | |
|---|---|---|---|---|---|
| 📄 | New Evidence | $0.390 | ▲ 2.0% | evidence_batch_update | 2026-04-13 02:18 |
| 📄 | New Evidence | $0.383 | ▲ 5.1% | evidence_batch_update | 2026-04-13 02:18 |
| ⚖ | Recalibrated | $0.364 | ▼ 0.6% | 2026-04-12 10:15 | |
| ⚖ | Recalibrated | $0.366 | ▼ 1.5% | 2026-04-10 15:58 | |
| ⚖ | Recalibrated | $0.372 | ▲ 1.8% | 2026-04-10 15:53 | |
| ⚖ | Recalibrated | $0.365 | ▼ 4.6% | 2026-04-08 18:39 | |
| ⚖ | Recalibrated | $0.383 | ▼ 15.3% | 2026-04-06 04:04 | |
| ⚖ | Recalibrated | $0.452 | ▼ 0.7% | 2026-04-04 16:38 | |
| ⚖ | Recalibrated | $0.455 | ▼ 1.1% | 2026-04-04 16:02 | |
| 📄 | New Evidence | $0.460 | ▲ 1.4% | evidence_batch_update | 2026-04-04 09:08 |
| ⚖ | Recalibrated | $0.454 | ▼ 1.9% | 2026-04-03 23:46 | |
| ⚖ | Recalibrated | $0.463 | ▲ 33.8% | 2026-04-02 21:55 | |
| 📊 | Score Update | $0.346 | ▼ 4.2% | market_dynamics | 2026-04-02 19:38 |
| ⚖ | Recalibrated | $0.361 | ▼ 2.7% | market_recalibrate | 2026-04-02 19:14 |
| 📄 | New Evidence | $0.371 | ▲ 3.8% | market_dynamics | 2026-04-02 18:45 |
Clinical Trials (6) Relevance: 45%
0
Active
Active
0
Completed
Completed
328
Total Enrolled
Total Enrolled
PHASE1
Highest Phase
Highest Phase
COMPLETED
·
NCT03317431 · Xinhua Hospital, Shanghai Jiao Tong University School of Medicine
46 enrolled · 2017-03-20 · → 2017-10-22
Dopamine(DA) is a common neurotransmitter that has been known to regulate behavior, movement, cardiovascular，endocrine and gastrointestinal functions, but also functions as an important molecule engag
Acute Lung Injury
mechanical ventilation
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 (44)
Ligand entry in human ileal bile acid-binding protein is mediated by histidine protonation.
Scientific reports (2019) · PMID:30886237
10 figures
Figure 1
( A ) Ribbon diagram of the heterotypic human I-BABP:GCDA:GCA complex determined by solution NMR (PDB entry 2MM3 6 ). Bound bile salts are shown in a ball-and-stick representation....
pmc_api
Figure 2
ITC analysis of the pH-dependence of bile salt binding to human I-BABP. Injection profiles for ( A ) GCA and ( B ) GCDA at pH = 7.2. The discontinuity at an x axis value of approxi...
pmc_api
Tyrosine hydroxylase (TH), its cofactor tetrahydrobiopterin (BH4), other catecholamine-related enzymes, and their human genes in relation to the drug and gene therapies of Parkinson's disease (PD): historical overview and future prospects.
Journal of neural transmission (Vienna, Austria : 1996) (2016) · PMID:27491309
1 figure
Figures
Figures available at source paper (no open-access XML found).
deep_link
Reconstruction of cell spatial organization from single-cell RNA sequencing data based on ligand-receptor mediated self-assembly.
Cell research (2020) · PMID:32541867
8 figures
Fig. 1
Schematics of single-cell spatial reconstruction by CSOmap. a CSOmap takes the gene-by-cell expression matrix generated by scRNA-seq and the known ligand-receptor network as input...
pmc_api
Fig. 2
The exocrine and endocrine compartments of pancreas can be recapitulated by ligand-receptor based inference with CSOmap. a The 3D visualization of CSOmap prediction of the human p...
pmc_api
Assessment of neuroimaging techniques as biomarkers of the progression of Parkinson's disease.
Experimental neurology (2003) · PMID:14597329
1 figure
Figures
Figures available at source paper (no open-access XML found).
deep_link
Antiparkinson prodrugs.
Molecules (Basel, Switzerland) (2008) · PMID:18259129
24 figures
Scheme 1
Dopamine biosynthesis.
pmc_api
Figure 1
No caption available
pmc_api
Assessment of neuroimaging techniques as biomarkers of the progression of Parkinson's disease.
Experimental neurology (2003) · PMID:14597329
No extracted figures yet
Altered fractionation: a fractional benefit?
The Lancet (2006) · PMID:16950339
No extracted figures yet
Antiparkinson prodrugs.
Molecules (Basel, Switzerland) (2008) · PMID:18259129
No extracted figures yet
Reward and aversion in a heterogeneous midbrain dopamine system.
Neuropharmacology (2014) · PMID:23578393
No extracted figures yet
Differential modulation of innate immunity in vitro by probiotic strains of Lactobacillus gasseri.
BMC microbiology (2013) · PMID:24365457
No extracted figures yet
Large-scale meta-analysis of genome-wide association data identifies six new risk loci for Parkinson's disease.
Nature genetics (2014) · PMID:25064009
No extracted figures yet
Tyrosine hydroxylase (TH), its cofactor tetrahydrobiopterin (BH4), other catecholamine-related enzymes, and their human genes in relation to the drug and gene therapies of Parkinson's disease (PD): historical overview and future prospects.
Journal of neural transmission (Vienna, Austria : 1996) (2016) · PMID:27491309
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)
Tet Methylcytosine Dioxygenase 2 Protein proteinThalamocortical Pathway circuitYARS2 — Tyrosyl-tRNA Synthetase 2, Mitochondrial geneApoptosis Pathways in Alzheimer's Disease mechanismNucleus of the Diagonal Band - Vertical Limb cellPDGFRA - Platelet Derived Growth Factor Receptor A geneAD/PD Therapeutic Target Comparison Matrix therapeuticMultiple Sclerosis Mechanistic Pathway mechanismSMO — Smoothened, Frizzled Class Receptor geneFGF2 — Fibroblast Growth Factor 2 geneLateral Hypothalamic Orexin Neurons in Narcolepsy cellNuclear Factor Erythroid 2-Related Factor 2 (Nrf2) proteinDorsomedial Hypothalamic Nucleus Neurons cellIGF2 Protein (Insulin-like Growth Factor 2) proteinExperiment: Autoimmune Hypothesis Testing in AD experiment
📓 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
16
Citations Produced
23
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
44298.70 tokens
Tokens / composite_score
Score Impact
Efficiency Boost to Composite
+0.049
10% weight of efficiency score
Adjusted Composite
0.433
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 | $0.383 | 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 TH, AADC.
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
Tet Methylcytosine Dioxygenase 2 ProteinproteinThalamocortical PathwaycircuitYARS2 — Tyrosyl-tRNA Synthetase 2, MitochondrialgeneApoptosis Pathways in Alzheimer's DiseasemechanismNucleus of the Diagonal Band - Vertical LimbcellPDGFRA - Platelet Derived Growth Factor Receptor AgeneAD/PD Therapeutic Target Comparison MatrixtherapeuticMultiple Sclerosis Mechanistic PathwaymechanismSMO — Smoothened, Frizzled Class ReceptorgeneFGF2 — Fibroblast Growth Factor 2geneLateral Hypothalamic Orexin Neurons in NarcolepsycellNuclear Factor Erythroid 2-Related Factor 2 (Nrf2)proteinDorsomedial Hypothalamic Nucleus NeuronscellIGF2 Protein (Insulin-like Growth Factor 2)proteinExperiment: Autoimmune Hypothesis Testing in ADexperiment
KG Entities (14)
GLP1_receptorNLRP3Parkinsons_diseaseSCFA_productionblood_brain_barriergut_microbiomeinflammasome_complexintestinal_barrierneuroinflammation_pathwayneuroprotectionprocessedsess_SDA-2026-04-01-gap-20260401-225155tight_junction_proteinsvagal_signaling_pathway
Linked Experiments (1)
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
3.5 years
🧪 Falsifiable Predictions (3)
3 total
0 confirmed
0 falsified
If hypothesis is true, intervention inhibit bacterial growth through feedback mechanisms
pending
conf: 0.20
Expected outcome: inhibit bacterial growth through feedback mechanisms
Falsified by: Intervention fails to inhibit bacterial growth through feedback mechanisms
If hypothesis is true, intervention effectively restore dopaminergic signaling in 6-OHDA-treated neuronal cultures, with 70-80% recovery of tyrosine hydroxylase-positive cell populations
pending
conf: 0.20
Expected outcome: effectively restore dopaminergic signaling in 6-OHDA-treated neuronal cultures, with 70-80% recovery of tyrosine hydroxylase-positive cell populations
Falsified by: Intervention fails to effectively restore dopaminergic signaling in 6-OHDA-treated neuronal cultures, with 70-80% recovery of tyrosine hydroxylase-positive cell populations
If hypothesis is true, intervention prioritize patients with demonstrated L-DOPA responsiveness but emerging motor fluctuations, as this population represents the optimal risk-benefit profile for initial studies
pending
conf: 0.20
Expected outcome: prioritize patients with demonstrated L-DOPA responsiveness but emerging motor fluctuations, as this population represents the optimal risk-benefit profile for initial studies
Falsified by: Intervention fails to prioritize patients with demonstrated L-DOPA responsiveness but emerging motor fluctuations, as this population represents the optimal risk-benefit profile for initial studies
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 TH, AADC
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
🧬 TH — PDB 1TOH 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