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30 results

Wiki Validated Hypothesis: p38α Inhibitor and PRMT1 Activator Combination to Restore Physiological TDP-43 Phosphorylation-Methylation Balance rel 6.19

TDP-43 hyperphosphorylation was established early in TDP-43 biology

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Wiki Validated Hypothesis: HSPB1 Phosphorylation Mimetics to Promote Protective TDP-43 Liquid-Liquid Phase Separation rel 4.45

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

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Wiki TDP-43 Causal Weight Analysis: Motor-Neuron Loss in ALS and FTD-TDP rel 3.88

TDP-43^ΔNLS) that mislocalize TDP-43 without forcing aggregation

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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 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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Wiki Validated Hypothesis: Microglial AIM2 Inflammasome as the Primary Driver of TDP-43 Proteinopathy Neuroinflammation in ALS/FTD rel 2.54

TDP-43 Proteinopathy Neuroinflammation in ALS/FTD > **Status**: ✅ Validated | **Composite

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Wiki Validated Hypothesis: TDP-43 RNA-proteostasis failure across ALS, FTD, and AD/LATE rel 2.42

TDP-43 construct; quantify nuclear/cytoplasmic TDP-43, cryptic exon burden

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Wiki Validated Hypothesis: TIA1 Low-Complexity Domain Oxidation Drives Aberrant Stress Granule Assembly and TDP-43 Mislocalization in ALS Motor Neurons rel 2.39

TDP-43 aggregation, distinct from downstream strategies targeting established TDP

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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 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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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 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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Paper The Pathobiology of TDP-43 C-Terminal Fragments in ALS and FTLD. rel 1.81

TDP-43 CTF cell culture models. Furthermore, TDP-43 CTF expression

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Hypothesis Enhanced MCU Activity Primes mPTP Opening in Motor Neurons rel 1.78

TDP-43 models, maintaining normal mitochondrial aspect ratios (3.2±0.4 vs 1.8±0.3 in TDP

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Hypothesis Autophagy-Lysosomal Flux Impairment Preventing Pathological TDP-43 Clearance rel 1.78

TDP-43 clearance co-localization data from FTLD, not AD-TDP

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Hypothesis Astrocytic APOE4 Disruption of GABAergic Support Increasing Neuronal Vulnerability rel 1.75

TDP-43 pathology. The proposed pathway connects astrocytic APOE4 to GLT-1 glutamate

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Wiki Validated Hypothesis: RBM45 Liquid-Liquid Phase Separation Dominance Hijacks RNA Processing Condensates Toward Pathological Aggregation in ALS rel 1.64

TDP-43,TARDBP,hnRNP A1,HNRNPA1,phase separation,Liquid droplet

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Hypothesis Synaptic RNA Metabolism Dysregulation rel 1.63

TDP-43 accumulation in AD neurons disrupts normal nuclear function

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Hypothesis VDAC1 Hyper-Oligomerization via Direct TDP-43 Binding rel 1.54

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

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Hypothesis G3BP1-TDP-43 Cross-Seeding Drives Co-Aggregation That Prion-Spreads Across Neural Circuits rel 1.53

TDP-43 co-condenses with G3BP1 in stress granules, altering

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Hypothesis Necroptosis-cGAS Feedforward Loop Converts TDP-43 Pathology into Neuroinflammation rel 1.53

TDP-43 Pathology into Neuroinflammation starts from the claim that

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Wiki Validated Hypothesis: STING Antagonists as ALS Therapeutics: Drug Repurposing rel 1.52

TDP-43 (TAR DNA-binding protein 43) pathology - a hallmark

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