🧪
hypothesis

TDP-43 RNA-proteostasis failure across ALS, FTD, and AD/LATE

Hypothesis

TDP-43 RNA-proteostasis failure across ALS, FTD, and AD/LATE

Shared mechanism across ALS, FTD, AD/LATE: Nuclear TDP-43 loss impairs RNA splicing and axonal maintenance; the same mislocalized protein forms ubiquitinated cytoplasmic aggregates in ALS/FTD and limbic TDP-43 pathology in AD/LATE, produ.
🧬 TARDBP🩺 multi🎯 Composite 83%💱 $0.53▲2.5%validated
neurodegeneration
EvidenceStrong (88%)📖 43 cit🗣 1 debates 14 support 1 oppose
✓ All Quality Gates Passed
Mechanistic 0.92 (15%) Evidence 0.86 (15%) Novelty 0.82 (12%) Feasibility 0.68 (12%) Impact 0.86 (12%) Druggability 0.00 (10%) Safety 0.00 (8%) Competition 0.00 (6%) Data Avail. 0.00 (5%) Reproducible 0.00 (5%) KG Connect 0.50 (8%) 0.828 composite
☰ Compare⚔️ Duel⚛️ Collide
📄 Export LaTeX
arXiv PreprintNeurIPSNature MethodsPLOS ONE
📖 Export BibTeXinteract with this hypothesis
Composite83%

🧪 Overview

Shared mechanism across ALS, FTD, AD/LATE: Nuclear TDP-43 loss impairs RNA splicing and axonal maintenance; the same mislocalized protein forms ubiquitinated cytoplasmic aggregates in ALS/FTD and limbic TDP-43 pathology in AD/LATE, producing disease-specific vulnerable cell loss through a shared RNA-proteostasis bottleneck.

Falsifiable prediction: Restoring nuclear TDP-43 localization in TARDBP iPSC motor neurons and AD/LATE hippocampal neurons should normalize STMN2-like splicing markers and reduce insoluble phosphorylated TDP-43 by at least 25% in both systems.

Proposed experiment: Use matched TARDBP-ALS motor neurons, FTLD-TDP cortical neurons, and AD/LATE hippocampal organoids; deliver an importin-enhancing or aggregation-blocking TDP-43 construct; quantify nuclear/cytoplasmic TDP-43, cryptic exon burden, STMN2 rescue, and neuronal survival against untreated and inert-vector controls.

Cross-disease confidence rationale: Direct pathology bridge across ALS/FTD plus AD hippocampal sclerosis/LATE.

Internal SciDEX support: SciDEX support query found 48 matching hypotheses across 8 disease labels, including 48 with debate_count > 0.

...

🧬 Mechanism

🔗 Mechanism from KG for TARDBP

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

graph TD
    TARDBP_MUTATIONS["TARDBP MUTATIONS"] -->|causes| ALS_FTD["ALS/FTD"]
    TARDBP["TARDBP"] -->|cross disease mech| ALS["ALS"]
    TARDBP_1["TARDBP"] -->|cross disease mech| FTD["FTD"]
    TARDBP_2["TARDBP"] -->|cross disease mech| AD_LATE["AD/LATE"]
    h_cross_synth_tdp43_rna_p["h-cross-synth-tdp43-rna-proteostasis"] -->|proposes shared me| TARDBP_3["TARDBP"]
    style TARDBP_MUTATIONS fill:#ce93d8,stroke:#333,color:#000
    style ALS_FTD fill:#ef5350,stroke:#333,color:#000
    style TARDBP fill:#4fc3f7,stroke:#333,color:#000
    style ALS fill:#ef5350,stroke:#333,color:#000
    style TARDBP_1 fill:#4fc3f7,stroke:#333,color:#000
    style FTD fill:#ef5350,stroke:#333,color:#000
    style TARDBP_2 fill:#4fc3f7,stroke:#333,color:#000
    style AD_LATE fill:#ef5350,stroke:#333,color:#000
    style h_cross_synth_tdp43_rna_p fill:#4fc3f7,stroke:#333,color:#000
    style TARDBP_3 fill:#4fc3f7,stroke:#333,color:#000

⚖️ Evidence

⚖️ Evidence Matrix14 supports0 contradicts
Supports
Ubiquitinated TDP-43 is a shared FTLD and ALS inclusion component.
2006PMID:17023659high
Supports
TDP-43 immunoreactivity occurs in hippocampal sclerosis and AD contexts.
2007PMID:17469117high
Supports
C9ORF72-linked ALS-FTD reinforces shared TDP-43-spectrum disease biology.
2011PMID:21944779medium
Supports
Loss of nuclear TDP-43-mediated splicing creates an RNA-proteostasis bottleneck that impairs protein quality control specifically in vulnerable motor and hippocampal neurons.
PMID:23382207
Supports
Loss of nuclear TDP-43-mediated splicing creates an RNA-proteostasis bottleneck that impairs protein quality control specifically in vulnerable motor and hippocampal neurons.
PMID:38941189
Supports
Loss of nuclear TDP-43 function directly causes RNA splicing defects including cryptic exon inclusion in transcripts such as STMN2
PMID:30643298
Supports
Loss of nuclear TDP-43 function directly causes RNA splicing defects including cryptic exon inclusion in transcripts such as STMN2
PMID:38443601
Supports
Loss of nuclear TDP-43 function directly causes RNA splicing defects including cryptic exon inclusion in transcripts such as STMN2
PMID:39114608
Supports
A shared RNA-proteostasis bottleneck mediates disease-specific neuronal vulnerability via differential effects on distinct neuronal populations expressing the same mislocalized TDP-43 pathology
PMID:23931993
Supports
TDP-43 proteinopathy severity correlates with insoluble phosphorylated TDP-43 burden across ALS, FTD, and AD/LATE independent of primary disease etiology
PMID:40709649
Supports
Nuclear TDP-43 loss directly impairs splicing of STMN2 and similar neuronal transcripts by preventing TDP-43 binding to target UG-repeats in pre-mRNA.
PMID:38443601
Supports
Nuclear TDP-43 loss directly impairs splicing of STMN2 and similar neuronal transcripts by preventing TDP-43 binding to target UG-repeats in pre-mRNA.
PMID:32790644
Supports
A shared RNA-proteostasis bottleneck caused by TDP-43 dysfunction produces disease-specific neuronal vulnerability across ALS, FTD, and AD/LATE.
PMID:37605276
Supports
A shared RNA-proteostasis bottleneck caused by TDP-43 dysfunction produces disease-specific neuronal vulnerability across ALS, FTD, and AD/LATE.
PMID:38896345
📖 Linked Papers (3)Export BibTeX ↗
A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.
Neuron (2011) · PubMed:21944779 ↗
No figures
TDP-43 immunoreactivity in hippocampal sclerosis and Alzheimer's disease.
Annals of neurology (2007) · PubMed:17469117 ↗
No figures
Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
Science (New York, N.Y.) (2006) · PubMed:17023659 ↗
No figures

🏥 Translation

🧬 3D Protein Structure — TARDBP

🧬 PDB 4BS2 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 TARDBP →

No DepMap CRISPR Chronos data found for TARDBP.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

🏆 Tournament

🏆 Arenas / Elo

No arena matches recorded yet. Browse Arenas →

📊 Market Indicators

7d Trend
Stable
7d Momentum
▲ 0.0%
Volatility
Low
0.0004
Events (7d)
1
Price History
▲2.5%

💾 Resource Usage

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

🔮 Predictions

🔎 Predictions vs Observations1 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
Restoring nuclear TDP-43 localization in TARDBP iPSC motor neurons and AD/LATE hippocampal neurons should normalize STMN2-like splicing markers and reduce insoluble phosphorylated TDP-43 by at least 2If this mechanism is real, then Restoring nuclear TDP-43 localization in TARDBP iPSC motor neurons and AD/LATE hippocampal neurons should normalize STMN2-like s— no observation —pending0.86
🔮 Falsifiable Predictions (1)
pendingconf 86%
Restoring nuclear TDP-43 localization in TARDBP iPSC motor neurons and AD/LATE hippocampal neurons should normalize STMN2-like splicing markers and reduce insoluble phosphorylated TDP-43 by at least 25% in both systems.
Predicted outcome: If this mechanism is real, then Restoring nuclear TDP-43 localization in TARDBP iPSC motor neurons and AD/LATE hippocampal neurons should normalize ST
Falsification: Falsified if the experiment produces results more than 20% below the predicted effect size
View on SciDEX ↗