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✓ 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 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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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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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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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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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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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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Hypothesis Glial Neuroinflammatory Amplification by TDP-43 Pathology rel 1.44

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

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Hypothesis Age-dependent downregulation of KPNA2 creates limbic neuron-specific nuclear import deficiency for TDP-43, explaining the predilection for hippocampal/amygdala pathology in AD versus motor neuron predominance in ALS rel 1.41

TDP-43, explaining the predilection for hippocampal/amygdala pathology in AD versus

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Hypothesis Tau Cross-Seeding and Interaction rel 1.33

TDP-43 burden in limbic regions. [PMID:34930382]. 3. TDP

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Hypothesis STING Antagonists as ALS Therapeutics: Drug Repurposing rel 1.32

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

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Hypothesis Liquid-to-Solid Transition Pathology Reveals Granule Weak Points rel 1.22

TDP-43 and FUS within granule-enriched fractions. The TDP

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Hypothesis MCU Calcium Overload via MFN2/GRP75/VDAC1 MAM Dysfunction rel 1.22

TDP-43 models. [PMID:35839797]. 2. Whether TDP-43 causes

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Hypothesis Direct APOE4-TDP-43 Protein-Protein Interaction Promoting Aggregation Seeding rel 1.22

TDP-43, acting as a scaffold that facilitates liquid-liquid

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Hypothesis Drp1-S616 Phosphorylation Fission Priming Enables t-Bid-Driven MPTP Amplification rel 1.11

TDP-43 engages stress kinases (PKCδ, CDK5, or GSK3β) to phosphorylate

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Hypothesis TIA1 Low-Complexity Domain Oxidation Drives Aberrant Stress Granule Assembly and TDP-43 Mislocalization in ALS Motor Neurons rel 1.08

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

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Hypothesis TBK1 Loss Drives MMP-9-Mediated TDP-43 Fragmentation Through Senescent Microglial SASP rel 1.06

TDP-43 aggregation. The fragmented TDP-43 species exhibit enhanced

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Hypothesis SASP-Secreted MMP-9 from Senescent Microglia Generates Pathological TDP-43 C-Terminal Fragments That Propagate ALS Pathology rel 1.04

TDP-43) that propagate ALS pathology through cytoplasmic aggregation seeding

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