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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 STING Antagonism Prevents Acute-to-Chronic Neuroinflammation Transition via Interruption of IFN-I Feedback Looping rel 2.20

Neuroinflammation Transition via Interruption of IFN-I Feedback Looping starts

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Hypothesis Necroptosis-cGAS Feedforward Loop Converts TDP-43 Pathology into Neuroinflammation rel 2.20

Neuroinflammation starts from the claim that modulating MLKL / RIPK1 within

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Hypothesis Testosterone-Derived DHT Amplifies Microglial Androgen Receptor Signaling Driving Male-Biased Neuroinflammation rel 2.10

Neuroinflammation starts from the claim that modulating AR within the disease

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Hypothesis Astrocyte cGAS/STING Activation Converts Protective into Destructive Neuroinflammation rel 2.10

Neuroinflammation starts from the claim that modulating STING (TMEM173) in astrocytes

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Hypothesis Age-related neuroinflammation mimics early Alzheimer's disease pathology rel 2.10

neuroinflammation mimics early Alzheimer's disease pathology starts from the claim

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Hypothesis Systemic IL-6–STAT3–Hepatic C3 Axis and BBB-Mediated Complement Translocation rel 1.90

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis GAS6/TAM Axis Activation Stabilizes Blood-Brain Barrier to Reduce Neuroinflammatory Cell Infiltration in Alzheimer's Disease rel 1.80

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Age-Accelerated miR-155 Upregulation Primes Nigral Microglia for Parkinson's Disease Pathology rel 1.70

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis CX3CR1-Negative Trem2-High Microglial Subset Mediates Female Resilience via Estrogen Receptor-alpha Suppression of NLRP3 rel 1.70

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Microglial AIM2 Inflammasome as the Primary Driver of TDP-43 Proteinopathy Neuroinflammation in ALS/FTD rel 1.70

Neuroinflammation in ALS/FTD starts from the claim that modulating AIM2

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Hypothesis C1Q-Glia Cross-Talk in Vascular Dementia Pathogenesis rel 1.70

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis NETosis Amplification by C1Q in Plaque Neutrophils rel 1.70

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Paraneoplastic myelopathies involve CD8+ T cell recognition of viral/cancer antigens causing necroptotic neuronal death rel 1.50

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis P2RY12/P2RY13 Purinergic Receptor Metabolic Rewiring rel 1.50

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Chronic cGAS/STING Hyperactivation Drives Progressive Neurodegeneration Through Sustained Type I Interferon Signaling rel 1.50

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis CD44-Mediated Src/PI3K/Akt Signaling Cascade rel 1.50

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis α4β1 Integrin (VLA-4) and JAK/STAT Pathway rel 1.50

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis TAM Receptor (MERTK/AXL) Cross-Regulation rel 1.50

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis MOG-IgG induces spinal cord demyelination through Fcγ receptor-dependent macrophage activation rel 1.50

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Mitochondrial DAMPs-Driven AIM2 Inflammasome Activation in Neurodegeneration rel 1.50

neuroinflammation and cellular damage. ## Preclinical Evidence Multiple lines of preclinical

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Hypothesis Temporal cGAS-STING Activation Stage-Specific Therapeutic Targeting rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Disease-Associated Microglia (DAM) Program Drives IBA1 Downregulation rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Microglial priming is primarily epigenetic, with metabolic changes acting as coupled consequences or cofactors rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis PKM2 nuclear translocation bridges metabolism and inflammatory transcription in primed microglia rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis BMAL1-CLOCK regulation of miR-143/145 locks microglia into glycolytic priming rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Primed microglia occupy a hybrid high-glycolysis and high-respiration metabolic state rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis ISG Threshold Model Explains Acute vs Chronic Neurodegeneration Outcomes rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Microglial Membrane Camouflage Exploits CD47-SIRPα Checkpoint Disinhibition rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Metabolic Accumulation (Ammonia/Manganese) Triggers IBA1 Downregulation via NRF2 rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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Hypothesis Regional TREM2-Dependent Lipid Metabolism Determines Cortical Vulnerability in Alzheimer's Disease rel 1.40

neuroinflammation can redirect a disease-relevant process. The original description

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