🧪
hypothesis

Combinatorial PTM signatures distinguish pathological from physiological tau states

Hypothesis

Combinatorial PTM signatures distinguish pathological from physiological tau states

A quantitative threshold of phosphorylation (S396/S404), acetylation (K280), and truncation (D421) defines a pathological tau PTM signature that predicts therapeutic vulnerability better than any single modification alone.
🧬 MAPT🩺 neurodegeneration🎯 Composite 46%💱 $0.53▲7.2%active
EvidencePending (0%)📖 5 cit🗣 1 debates 5 support 1 oppose
✓ All Quality Gates Passed
Mechanistic 0.50 (15%) Evidence 0.50 (15%) Novelty 0.50 (12%) Feasibility 0.50 (12%) Impact 0.00 (12%) Druggability 0.50 (10%) Safety 0.50 (8%) Competition 0.50 (6%) Data Avail. 0.50 (5%) Reproducible 0.50 (5%) KG Connect 0.24 (8%) 0.455 composite
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arXiv PreprintNeurIPSNature MethodsPLOS ONE
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Composite46%

🧪 Overview

A quantitative threshold of phosphorylation (S396/S404), acetylation (K280), and truncation (D421) defines a pathological tau PTM signature that predicts therapeutic vulnerability better than any single modification alone.

🧬 Mechanism

🔗 Mechanism from KG for MAPT

Auto-built from this analysis's top knowledge-graph edges.

graph TD
    tau_protein["tau_protein"] -->|undergoes| post_translational_modifi["post_translational_modifications"]
    post_translational_modifi_1["post_translational_modifications"] -->|contributes to| pathological_tau["pathological_tau"]
    pathological_tau_2["pathological_tau"] -->|causes| neurodegeneration["neurodegeneration"]
    CASP2["CASP2"] -->|causes| TAU_Aggregation["TAU Aggregation"]
    CASP3["CASP3"] -->|causes| TAU_Aggregation_3["TAU Aggregation"]
    EP300["EP300"] -->|causes| K280_acetylated_tau["K280 acetylated tau"]
    D421_truncation["D421 truncation"] -->|biomarker for| Alzheimer_s_disease["Alzheimer's_disease"]
    K280_acetylation["K280 acetylation"] -->|associated with| Alzheimer_s_disease_4["Alzheimer's_disease"]
    CASP2_5["CASP2"] -->|causes| Neurofibrillary_Tangle_Fo["Neurofibrillary Tangle Formation"]
    EP300_6["EP300"] -->|regulates| TAU_Acetylation["TAU Acetylation"]
    post_translational_modifi_7["post_translational_modifications"] -->|causes| pathological_tau_8["pathological_tau"]
    sess_SDA_2026_04_09_gap_d["sess_SDA-2026-04-09-gap-debate-20260409-201742-1e8eb3bd_20260412-091129"] -->|causal extracted| processed["processed"]
    style tau_protein fill:#4fc3f7,stroke:#333,color:#000
    style post_translational_modifi fill:#81c784,stroke:#333,color:#000
    style post_translational_modifi_1 fill:#81c784,stroke:#333,color:#000
    style pathological_tau fill:#4fc3f7,stroke:#333,color:#000
    style pathological_tau_2 fill:#4fc3f7,stroke:#333,color:#000
    style neurodegeneration fill:#ef5350,stroke:#333,color:#000
    style CASP2 fill:#ce93d8,stroke:#333,color:#000
    style TAU_Aggregation fill:#4fc3f7,stroke:#333,color:#000
    style CASP3 fill:#ce93d8,stroke:#333,color:#000
    style TAU_Aggregation_3 fill:#4fc3f7,stroke:#333,color:#000
    style EP300 fill:#ce93d8,stroke:#333,color:#000
    style K280_acetylated_tau fill:#4fc3f7,stroke:#333,color:#000
    style D421_truncation fill:#4fc3f7,stroke:#333,color:#000
    style Alzheimer_s_disease fill:#ef5350,stroke:#333,color:#000
    style K280_acetylation fill:#4fc3f7,stroke:#333,color:#000
    style Alzheimer_s_disease_4 fill:#ef5350,stroke:#333,color:#000
    style CASP2_5 fill:#ce93d8,stroke:#333,color:#000
    style Neurofibrillary_Tangle_Fo fill:#4fc3f7,stroke:#333,color:#000
    style EP300_6 fill:#ce93d8,stroke:#333,color:#000
    style TAU_Acetylation fill:#4fc3f7,stroke:#333,color:#000
    style post_translational_modifi_7 fill:#4fc3f7,stroke:#333,color:#000
    style pathological_tau_8 fill:#4fc3f7,stroke:#333,color:#000
    style sess_SDA_2026_04_09_gap_d fill:#4fc3f7,stroke:#333,color:#000
    style processed fill:#4fc3f7,stroke:#333,color:#000

⚖️ Evidence

⚖️ Evidence Matrix5 supports0 contradicts
Supports
Interactions between Microtubule-Associated Protein Tau (MAPT) and Small Molecules.
Cold Spring Harb Perspect Med2017PMID:27940599medium
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
Tau filaments with the Alzheimer fold in human MAPT mutants V337M and R406W.
Nat Struct Mol Biol2025PMID:40044789medium
Supports
Isoform-specific patterns of tau burden and neuronal degeneration in MAPT-associated frontotemporal lobar degeneration.
Acta Neuropathol2022PMID:36066634medium
📖 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*

💉 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 MAPT →

No DepMap CRISPR Chronos data found for MAPT.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

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📊 Market Indicators

7d Trend
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7d Momentum
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Volatility
Medium
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Events (7d)
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Price History
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💾 Resource Usage

LLM Tokens
17,312
$0.0625
Total Cost
$0.0625

🔮 Predictions

🔎 Predictions vs Observations2 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
IF human iPSC-derived cortical neurons are exposed to pathological seeds AND a combinatorial PTM threshold is met (phospho-S396/S404 ≥ 70% of total tau, acetyl-K280 ≥ 40%, and truncation at D421 ≥ 30%Combinatorial signature (+) cells show significantly higher tau seeding/aggregation readouts (e.g., FRET-based aggregation assay, Sarkosyl-insoluble tau fractio— no observation —pending0.68
IF preclinical cohorts of P301S transgenic mice are stratified by the combinatorial tau PTM signature (threshold as defined above) versus single-modification stratification prior to anti-tau antibody Mice meeting the full combinatorial signature show superior therapeutic response to anti-tau intervention, as measured by 50% reduction in Sarkosyl-insoluble ta— no observation —pending0.55
🔮 Falsifiable Predictions (2)
pendingconf 68%
IF human iPSC-derived cortical neurons are exposed to pathological seeds AND a combinatorial PTM threshold is met (phospho-S396/S404 ≥ 70% of total tau, acetyl-K280 ≥ 40%, and truncation at D421 ≥ 30% detected by targeted MS), THEN these neurons will exhibit ≥3-fold higher tau aggregation efficiency
Predicted outcome: Combinatorial signature (+) cells show significantly higher tau seeding/aggregation readouts (e.g., FRET-based aggregation assay, Sarkosyl-insoluble t
Falsification: Neurons with single PTM elevation (e.g., phospho-S396/S404 only, without acetylation or truncation) show equivalent aggregation efficiency to the combinatorial signature group, eliminating the added v
pendingconf 55%
IF preclinical cohorts of P301S transgenic mice are stratified by the combinatorial tau PTM signature (threshold as defined above) versus single-modification stratification prior to anti-tau antibody treatment (e.g., AJ196), THEN the combinatorial-stratified group will show ≥40% improvement in thera
Predicted outcome: Mice meeting the full combinatorial signature show superior therapeutic response to anti-tau intervention, as measured by 50% reduction in Sarkosyl-in
Falsification: Mice stratified by a single PTM marker (e.g., phospho-S396/S404 alone) show equivalent or superior therapeutic response to the combinatorial stratification group, indicating the combinatorial approach
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