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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 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 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 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 P2RY12/P2RY13 Purinergic Receptor Metabolic Rewiring 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 TAM Receptor (MERTK/AXL) Cross-Regulation 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 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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Hypothesis Female Microglia Exhibit Reduced P2Y12 Expression Conferring Neuroprotection Through Attenuated Chemotaxis rel 1.40

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

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Hypothesis Early Postnatal TGF-beta Signaling Establishes Lifelong Regional Vulnerability Through Irreversible Transcriptional Imprinting rel 1.40

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

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Hypothesis APOE4 Induces Region-Specific Microglial Senescence Driving Frontal Cortex Neurodegeneration rel 1.40

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

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Hypothesis αvβ3 Integrin-FAK-SYK-CARD9/NF-κB Pathway rel 0.90

neuroinflammation. **Preclinical Evidence** Preclinical validation of this pathway has emerged

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Hypothesis Microglial Disease-Associated States: TREM2-Independent Pathways Driving Neuroinflammation rel 0.70

Neuroinflammation starts from the claim that modulating APOE within the disease

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Hypothesis NLRP3 Inflammasome Lock Perpetuates Senescence-Associated Inflammasome Phenotype rel 0.60

neuroinflammation. The molecular cascade begins when aged microglia encounter diverse

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Hypothesis CD36 Acts as Primary Aβ Oligomer Sensor on Perivascular Macrophages, Triggering NF-κB-Dependent SPP1 Transcription rel 0.60

neuroinflammation, disrupts perivascular drainage, and contributes to the chronic neuroinflammatory

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Hypothesis TREM2 Agonism to Rescue APOE4-Induced Microglial Dysfunction rel 0.50

neuroinflammation, while insufficient activation may fail to overcome APOE4-mediated

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Hypothesis Galectin-3 deletion attenuates NLRP3 inflammasome activation downstream of lysosomal membrane permeabilization rel 0.50

neuroinflammation that may persist long after the initial insult, contributing

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Hypothesis P2X7/P2Y12 Purinergic Signaling Connects Aβ Aggregation to SPP1 Transcription via Calcineurin/NFAT Pathway rel 0.50

neuroinflammation and cognitive deficits. 2. **P2Y12 antagonists**: Clopidogrel, prasugrel, ticagrelor

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Hypothesis TREM2 haploinsufficiency dysregulates microglial synaptic surveillance, switching from protective 'disease-associated microglia' to neurotoxic 'inflammasome-active' states rel 0.40

neuroinflammation and accelerated age-related neurodegeneration. These cross-species validations

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Hypothesis IGFBPL1 Peptide Mimetics for Drug-Like BBB Permeability rel 0.40

neuroinflammation; neuroprotection against Aβ toxicity 2. **Parkinson's disease**: Neuroprotection

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Hypothesis LDLR-Mediated Neuroinflammation Modulation Strategy rel 0.40

Neuroinflammation Modulation Strategy proposes that direct pharmacological enhancement of LDLR

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Hypothesis LRP1-Autophagy BBB Permeabilization for Antibody Transport rel 0.40

neuroinflammation from unintended peripheral immune cell infiltration outweighs potential benefits

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Hypothesis EZH2-Mediated H3K27me3 Spreading in Senescent ALS Microglia Silences Neuroprotective Gene Programs — Reversible by EZH2 Inhibitors rel 0.40

neuroinflammation through the SOCS3/TRAF6/NF‑κB signaling axis and that this

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Hypothesis ω-3 Docosahexaenoic Acid (DHA) Metabolism via 15-Lipoxygenase to Generate Specialized Pro-Resolving Mediators Against Neuroinflammation in Alzheimer's Disease rel 0.40

neuroinflammation in Alzheimer's disease rather than focusing on membrane

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Hypothesis TREM2-Dependent Astrocyte-Microglia Cross-talk in Neuroinflammation rel 0.40

Neuroinflammation proposes that TREM2 dysfunction disrupts critical intercellular communication networks

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Hypothesis NeuroD1-Mediated Astrocyte Reprogramming Attenuates Neuroinflammation Through Epigenetic Remodeling of A1 Astrocyte Signature Genes rel 0.30

neuroinflammation to identify optimal candidates. The invasive nature of stereotactic

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Hypothesis Mitochondrial DNA Damage and cGAS-STING Activation Induces Microglial Senescence rel 0.30

neuroinflammation in PD models. [PMID:32424312]. 3. Aged microglia show

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Hypothesis TREM2 Deficiency Drives Microglial Senescence via Lipid Metabolism Dysregulation rel 0.30

neuroinflammation and accelerating neurodegeneration. **Preclinical Evidence** Extensive preclinical validation supports

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Hypothesis LDLR-Targeted Anti-Inflammatory Antibody Delivery for Neuroinflammation Suppression rel 0.30

neuroinflammation by combining reliable CNS delivery with targeted suppression of the glial

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