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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 P2RY12-mediated cerebral VSMC dysfunction establishes a vicious cycle with microglial P2RY12 activation rel 3.00

microglia) within the disease context of neurodegeneration can redirect a disease

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Hypothesis TREM2-Mediated Oligodendrocyte-Microglia Signaling in White Matter Neurodegeneration rel 2.00

microglia signaling axis represents a sophisticated cellular communication network essential

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Hypothesis Severely Depleted mtDNA and Impaired OXPHOS Defines Senescent Microglia rel 2.00

Microglia starts from the claim that Senescent microglia exhibit cumulative

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Hypothesis TREM2-Senescence Cascade in Astrocyte-Microglia Communication Breakdown rel 1.90

microglia communication networks. Healthy TREM2+ microglia communicate threat status to astrocytes

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Hypothesis Epigenetic Bivalency at CDKN2A Locus Distinguishes Senescent from Activated Microglia rel 1.80

Microglia starts from the claim that modulating CDKN2A, H3K9me3, DREAM

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Hypothesis CSF1R Inhibition Reversal Window Depends on Microglia Replacement Kinetics rel 1.80

Microglia Replacement Kinetics starts from the claim that modulating CSF1R

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Hypothesis CD36 Acts as Primary Aβ Oligomer Sensor on Perivascular Macrophages, Triggering NF-κB-Dependent SPP1 Transcription rel 1.80

microglia" phenotype — activated microglia with processes that encircled synapses and Aβ plaques

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Hypothesis TREM2-Mediated Oligodendrocyte-Microglia Cross-talk in White Matter Neurodegeneration rel 1.70

microglia from EAE lesions demonstrates that TREM2-deficient microglia fail

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Hypothesis Female microglia exhibit heightened complement gene expression and pruning capacity via estrogen-regulated epigenetic sensitization, explaining the female AD risk advantage rel 1.70

microglia exhibit heightened complement gene expression and pruning capacity via estrogen

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Hypothesis Persistent γH2AX+53BP1 Foci with DREAM Complex Activation Defines Irreversibly Arrested Microglia rel 1.70

Microglia starts from the claim that Senescent microglia accumulate persistent

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Hypothesis Microglial Replacement and Ontogeny Shift rel 1.70

microglia populate the central nervous system during embryonic development and self

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Hypothesis Autophagy-Lysosomal Degradation of IBA1 in Stressed Microglia rel 1.40

Microglia starts from the claim that modulating LC3/P62/SQSTM1 within the disease

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

microglia occupy a hybrid high-glycolysis and high-respiration metabolic

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Hypothesis Loss of Nuclear Lamin B1 Distinguishes Senescent Microglia from Inflammatory Activation rel 1.30

Microglia from Inflammatory Activation starts from the claim that modulating

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Hypothesis TREM2 haploinsufficiency dysregulates microglial synaptic surveillance, switching from protective 'disease-associated microglia' to neurotoxic 'inflammasome-active' states rel 1.30

microglia to disease-associated microglia (DAM), characterized by upregulation of genes

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Hypothesis TREM2-Dependent Senescent Microglia Disrupt Astrocyte Communication Networks rel 1.30

microglia within the central nervous system, where it functions as a pattern

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Hypothesis Mitochondrial DNA Damage and cGAS-STING Activation Induces Microglial Senescence rel 1.30

microglia. Framed more explicitly, the hypothesis centers CGAS/STING1/TMEM173 within the broader

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Hypothesis Temporal NLRP3 Inhibition via SPP1-Mediated Mitophagy Enhancement During Critical Neuroinflammatory Windows rel 1.20

microglia shift from homeostatic surveillance to maladaptive activation. During these

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Hypothesis Microglial Priming via NF-κB-Dependent DAM Phenotype and Complement Biosynthesis rel 1.20

microglia (DAM) phenotypes in neuroinflammatory conditions. The canonical NF-κB pathway

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Hypothesis Female Microglia Exhibit Reduced P2Y12 Expression Conferring Neuroprotection Through Attenuated Chemotaxis rel 1.20

Microglia Exhibit Reduced P2Y12 Expression Conferring Neuroprotection Through Attenuated Chemotaxis

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Hypothesis Selectively Inhibit Maladaptive AQP4-Driven Astrocyte-Microglia Inflammatory Signaling in Parkinsonian Injury rel 1.20

Microglia Inflammatory Signaling in Parkinsonian Injury starts from the claim

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Paper Patterns of Expression of Purinergic Receptor P2RY12, a Putative Marker for Non-Activated Microglia, in Aged and Alzheimer's Disease Brains. rel 1.20

microglia. Based on these results, P2RY12 expression by microglia should

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Paper Microglia in multiple sclerosis: Protectors turn destroyers. rel 1.20

Microglia are implicated in all stages of multiple sclerosis (MS). Microglia

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Paper Microglia in multiple sclerosis: Protectors turn destroyers. rel 1.20

Microglia are implicated in all stages of multiple sclerosis (MS). Microglia

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Hypothesis Loss of Homeostatic Epigenetic Identity Reprograms Microglia to Dystrophic State rel 1.10

Microglia to Dystrophic State starts from the claim that modulating

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Hypothesis Mitochondrial Damage-Triggered SPP1 Inflammasome Coupling rel 1.10

microglia creates a pathological coupling between SPP1 secretion and NLRP3

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Hypothesis Astrocytic SPP1 Modulation via STAT3-Dependent Transcriptional Control rel 1.10

microglia for sustained activation. This astrocytic SPP1 demonstrates preferential binding

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Hypothesis TREM2-Astrocyte Communication in Microglial Dysfunction rel 1.10

microglia within the central nervous system, where it associates with

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Hypothesis Temporal NLRP3 Inhibition During SPP1-Driven Microglial Activation Windows rel 1.10

microglia but also primes them for enhanced NLRP3 activation by upregulating

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Hypothesis Astrocytic SPP1 Modulation Through STAT3-Dependent Transcriptional Control rel 1.10

microglia, represent the primary pathogenic source of SPP1 in neuroinflammation

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