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All 7 Hypotheses 1 Papers 1 Wikis 1 Gaps 1 Colliders 0 Debates 1 Bounties 0 Missions 1 Work packets 1 Genes 0 Diseases 0 Phenotypes 0 Gene ontology 0

✓ Hypotheses 1 ✓ Papers 1 + Wikis 1 ✓ Gaps 1 + Colliders 0 + Debates 1 + Bounties 0 + Missions 1 + Work packets 1 + Genes 0 + Diseases 0 + Phenotypes 0 + Gene ontology 0

30 results

Hypothesis TDP-43 Cryptic Exon–Targeted ASOs to Restore Hippocampal Gamma Oscillations rel 6.59

TDP-43 involvement. Biomarker strategies, including cerebrospinal fluid TDP-43

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Hypothesis Arginine Methylation Enhancement Therapy rel 6.52

TDP-43. The TDP-43 protein contains multiple arginine-rich

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Hypothesis p38α Inhibitor and PRMT1 Activator Combination to Restore Physiological TDP-43 Phosphorylation-Methylation Balance rel 5.57

TDP-43 pathology, and p38α inhibition reduces pathological TDP-43

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Hypothesis Cross-Seeding Prevention Strategy rel 5.50

TDP-43-Aβ and TDP-43-tau interaction complexes in CSF, with

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Hypothesis PARP1 Inhibition Therapy rel 4.82

TDP-43). Under physiological conditions, TDP-43 functions as a nuclear

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Hypothesis Glycine-Rich Domain Competitive Inhibition rel 4.32

TDP-43 localization and normalized expression of TDP-43-regulated

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Hypothesis Serine/Arginine-Rich Protein Kinase Modulation rel 4.00

TDP-43 functionality. TDP-43 (TAR DNA-binding protein 43) is a predominantly

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Hypothesis HSPB1 Phosphorylation Mimetics to Promote Protective TDP-43 Liquid-Liquid Phase Separation rel 3.74

TDP-43 Liquid-Liquid Phase Separation ## Scientific Rationale TDP-43

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Hypothesis TSPO-Mediated TDP-43 Mitochondrial Import rel 3.68

TDP-43 Mitochondrial Import starts from the claim that modulating

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Hypothesis RNA Granule Nucleation Site Modulation rel 3.42

TDP-43 encephalopathy (LATE). Under physiological conditions, TDP-43 functions

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Hypothesis Low Complexity Domain Cross-Linking Inhibition rel 3.32

TDP-43. The low complexity domain of TDP-43, spanning

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Hypothesis Cryptic Exon Silencing Restoration rel 2.91

TDP-43 encephalopathy (LATE), and other TDP-43 proteinopathies affecting

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Hypothesis Aβ-induced downregulation of circPDS5B derepresses TDP-43 mRNA translation in limbic neurons, causing proteostatic overload and aggregation specifically in AD rel 2.58

TDP-43. Under physiological conditions, circPDS5B maintains homeostatic levels of TDP

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Hypothesis Nuclear Export Deficits Increase Cytosolic TDP-43 Burden rel 2.57

TDP-43 proteinopathy in neurodegenerative diseases. The central hypothesis revolves

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Hypothesis STMN2 Restoration as a Prerequisite for Axon Growth After TDP-43 Clearance rel 2.39

TDP-43 function and microtubule dynamics regulation. TDP-43 (TAR DNA-binding

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Hypothesis Nuclear TDP-43 Depletion Drives Synaptic Splicing Dysregulation in ALS-FTD rel 2.35

TDP-43 Depletion Drives Synaptic Splicing Dysregulation in ALS-FTD starts

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Paper TDP-43 Oligomerization and Phase Separation Properties Are Necessary for Autoregulation. rel 2.27

TDP-43 protein homeostasis and dysfunction, in particular TDP-43

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Hypothesis Cyclophilin D (CypD) Displacement by Mitochondrial TDP-43 rel 2.25

TDP-43 starts from the claim that Pathological TDP-43

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Hypothesis Heat Shock Protein 70 Disaggregase Amplification rel 2.20

TDP-43 fragments—reliable biomarkers of TDP-43 cleavage and aggregation

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Hypothesis Aβ42 oligomers drive TDP-43 phosphorylation at s409/410 through CDK5/p25 activation specifically in AD, generating a phospho-signature distinct from ALS/FTLD rel 2.19

TDP-43 and tau aggregation pathways, as phosphorylated TDP-43

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Hypothesis H3: G3BP1 as Nucleation Hub for TDP-43/FUS Seeding rel 2.07

TDP-43 in motor neurons, with approximately 70-80% of TDP

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Hypothesis DNA Damage Repair Dysfunction Creating TDP-43 Pathology Feed-Forward Loop rel 2.06

TDP-43 truncation (cTDP-43 fragments) that lose normal DNA repair

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Paper Tar DNA binding protein-43 (TDP-43) associates with stress granules: analysis of cultured cells and pathological brain tissue. rel 2.06

TDP-43 increased TDP-43 inclusion formation in response to stressful

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Paper ALS-linked TDP-43 mutations produce aberrant RNA splicing and adult-onset motor neuron disease without aggregation or loss of nuclear TDP-43. rel 2.04

TDP-43(Q331K) and TDP-43(M337V)), but not wild

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Hypothesis Cytosolic TDP-43 aggregation sequesters SNAP29 and syntaxin-17, blocking autophagosome-lysosome fusion rel 2.04

TDP-43 aggregation sequesters SNAP29 and syntaxin-17, blocking autophagosome

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Hypothesis Microglial AIM2 Inflammasome as the Primary Driver of TDP-43 Proteinopathy Neuroinflammation in ALS/FTD rel 2.03

TDP-43 Proteinopathy Neuroinflammation in ALS/FTD starts from the claim

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Paper Optineurin knock-out forms TDP-43 aggregates to regulate TDP-43 protein levels despite autophagic up-regulation and aberrant TDP-43 expression. rel 2.03

TDP-43-transgenic (TDP-43-tg) mice resulted in motor

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Hypothesis Mitochondrial Dysfunction Increasing Neuronal Vulnerability to TDP-43 Toxicity rel 1.94

TDP-43 Toxicity starts from the claim that modulating MCU, CK1D

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Hypothesis Neuroinflammation-Driven TDP-43 Mislocalization via Microglial APOE4 Signaling rel 1.87

TDP-43 localization by 4-6 weeks. Phosphorylated TDP-43

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Hypothesis Hyperphosphorylated TDP-43 Traps TRIM21 Into Inactive Complexes rel 1.84

TDP-43 Traps TRIM21 Into Inactive Complexes starts from the claim

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