ID: h-3ab2bff6a46b
Hypothesis

Repeat-domain exposure defines seed-competent tau conformers

Tau assemblies become seed-competent when their repeat-domain surfaces adopt a conformation that both survives transfer and templates monomeric tau into pathological aggregates.
🧬 MAPT🩺 neurodegeneration🎯 Composite 76%💱 $0.62▼24.1%proposed
EvidenceStrong (72%)📖 8 cit🗣 1 debates 8 support 2 oppose
✓ All Quality Gates Passed
Mechanistic 0.85 (15%) Evidence 0.73 (15%) Novelty 0.62 (12%) Feasibility 0.70 (12%) Impact 0.88 (12%) Druggability 0.61 (10%) Safety 0.66 (8%) Competition 0.55 (6%) Data Avail. 0.65 (5%) Reproducible 0.62 (5%) KG Connect 0.58 (8%) 0.760 composite
🏆 ChallengeSolve: Repeat-domain exposure defines seed-competent tau conformers$126K →

🧪 Overview

Tau assemblies become seed-competent when their repeat-domain surfaces adopt a conformation that both survives transfer and templates monomeric tau into pathological aggregates. This conformer-specific templating mechanism, supported by structural studies of disease-specific tau filaments, suggests that the exposed repeat domain interface is the critical determinant distinguishing pathogenic from non-pathogenic tau conformations. Non-pathogenic transferred tau lacks this exposed templating interface despite similar uptake, indicating that cellular internalization alone is insufficient for prion-like propagation. The probabilistic model of Alzheimer disease revised in 2022 suggests that such templated aggregation processes may be central to disease progression. Conformational exposure of the repeat domain thus defines seed-competent tau conformers and may represent a therapeutic target for preventing the establishment of the templating interface required for neurodegeneration.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
A["MAPT tau protein"]
B["Repeat domain conformational change"]
C["Exposed templating interface"]
D["Seed-competent tau conformer"]
E["Templating of monomeric tau"]
F["Survival during intercellular transfer"]
G["Non-pathogenic tau conformer"]
H["Lacks exposed interface"]
I["Propagation of tau aggregates"]
J["Neurodegeneration"]

A --> B
B --> C
C --> D
C --> G
D --> E
D --> F
E --> I
F --> I
I --> J
G --> H
H -.->|"No templating"| G

⚖️ Evidence

⚖️ Evidence Matrix6 supports1 contradicts
Supports
The probabilistic model of Alzheimer disease: the amyloid hypothesis revised.
Nat Rev Neurosci2022PMID:34815562
Supports
MAPT mutations, tauopathy, and mechanisms of neurodegeneration.
Lab Invest2019PMID:30742061medium
Supports
Tau-targeting antisense oligonucleotide MAPT(Rx) in mild Alzheimer's disease: a phase 1b, randomized, placebo-controlled trial.
Nat Med2023PMID:37095250medium
Supports
Interactions between Microtubule-Associated Protein Tau (MAPT) and Small Molecules.
Cold Spring Harb Perspect Med2017PMID:27940599medium
Supports
ELAVL4, splicing, and glutamatergic dysfunction precede neuron loss in MAPT mutation cerebral organoids.
Cell2021PMID:34314701medium
Supports
The six brain-specific TAU isoforms and their role in Alzheimer's disease and related neurodegenerative dementia syndromes.
Alzheimers Dement2024PMID:38556838medium
Contradicts
Alzheimer Disease: An Update on Pathobiology and Treatment Strategies.
📖 Linked Papers

No linked papers recorded for this hypothesis yet.

🏥 Translation

🧬 3D Protein Structure — MAPT

🧬 PDB 5O3L Click to expand

Experimental structure from RCSB PDB | Powered by Mol*

🧠 GTEx v10 Brain ExpressionJSON

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

Cerebellum209 Cerebellar Hemisphere199 Cortex152 Frontal Cortex BA9146 Anterior cingulate cortex BA24101 Hypothalamus86.4 Amygdala73.5 Nucleus accumbens basal ganglia72.2 Hippocampus72.1 Caudate basal ganglia64.7 Putamen basal ganglia58.1 Substantia nigra56.8 Spinal cord cervical c-149.2median TPM (GTEx v10)

💉 Clinical Trials (5)Relevance: 88%

0
Active
0
Completed
0
Total Enrolled
PHASE1
Highest Phase
COMPLETED·NCT06584656 · Universidad de Granada
Healthy Aging Cognitive Function 1, Social Cerebrovascular Circulation
Aerobic exercise condition Resistance exercise condition
COMPLETED·NCT01850238 · Axon Neuroscience SE
Alzheimer Disease
AADvac1 Placebo
RECRUITING·NCT04906863 · Columbia University
Dementia, Early Onset
Blood draw Neurocognitive testing Medical questionnaire
COMPLETED·NCT04413344 · Kyoto University
Familial Alzheimer Disease (FAD) PSEN1 Mutation
Bromocriptine Mesilate Placebos
COMPLETED·NCT03978052 · Parc de Salut Mar
Alzheimer Disease Cognitive Decline
EGCG Placebo EGCG Healthy lifestyle recommendations

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🔍 Search ClinVar for MAPT →

No DepMap CRISPR Chronos data found for MAPT.

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📊 Market Indicators

7d Trend
Stable
7d Momentum
▼ 1.9%
Volatility
Medium
0.0227
Events (7d)
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Price History
▼24.1%

💾 Resource Usage

No resource usage or linked notebooks recorded for this hypothesis yet.

Metadatasource: v1_phase_c_backfill · origin_type: gap_debate
sourcev1_phase_c_backfill
origin_typegap_debate
_schema_version1
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting 0 contradicting 0 neutral
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