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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 HK2-Dependent Metabolic Checkpoint as the Gatekeeper of DAM Transition rel 3.60

microglia to disease-associated microglia (DAM). This transition involves complex

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Hypothesis CSF1R Inhibition-Mediated Microglial Replacement as a State Transition Reset rel 3.10

microglia, with the highest expression in microglia bordering degenerating motor

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Hypothesis TREM2-APOE Axis Dissociation for Selective DAM Activation rel 3.00

Microglia cluster 1 ("homeostatic microglia"), co-expressing canonical markers including

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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 R47H Metabolic Lock-in at Cholesterol Ester Accumulation rel 2.70

microglia. Transcriptomic analyses of R47H iPSC-derived microglia demonstrate impaired

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Hypothesis TREM2 Agonism to Restore Microglial Phagocytosis Across Both Pathologies rel 2.70

microglia in the central nervous system, functioning as a master

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Hypothesis Selective Microglial Senescence Targeting via TREM2 Modulation rel 2.50

microglia stems from the observation that aged or dysfunctional microglia

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Hypothesis TREM2-mediated microglial tau clearance enhancement rel 2.10

microglia. They showed that TREM2-deficient microglia exhibited reduced uptake

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Hypothesis Temporal SPP1 Inhibition During Critical Windows rel 2.10

microglia (DAM) and aging-associated microglia. ### Animal Model Evidence Genetic

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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-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 TREM2-Microglial Clearance Enhancement as Common Mechanism for Injury Prevention rel 2.00

microglia to adopt a disease-associated microglia (DAM) or neurodegenerative

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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 Palmitoylethanolamide-Based Endocannabinoid Therapy rel 1.90

microglia reveals that aged microglia show reduced PPARA expression, potentially

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Hypothesis H1: TREM2 Agonism to Redirect APOE4-Enhanced Microglia from Synapse Pruning to Amyloid Clearance rel 1.90

Microglia from Synapse Pruning to Amyloid Clearance starts from the claim

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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 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 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 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 TREM2 Agonism to Redirect Microglia from Synaptic Pruning to OPTN-Deficient Neuron Protection rel 1.70

microglia (DAM) phenotype. Under physiological conditions, TREM2-expressing microglia participate

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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 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 Age-Dependent TREM2 Signaling Disrupts Astrocyte-Microglia Communication Leading to Senescent Glial Networks rel 1.70

microglia, this activation pattern promotes release of specific communication molecules

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Hypothesis Complement C1q Suppression as Mechanism Linking Exercise Plasma to PV Interneuron Protection rel 1.60

microglia, modulating their transcriptional programs and functional phenotypes. Microglia represent

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Hypothesis TYROBP Causal Network Inhibition for Microglial Repolarization rel 1.50

microglia, shifting them from a disease-associated microglia (DAM) state

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Hypothesis TREM2-Dependent Microglial Phagocytosis Acts as a Strain Selection Filter rel 1.50

microglia determines whether a given tau species undergoes complete proteolytic

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Hypothesis SYK-Independent TREM2 Pathways Remain Functional in TYROBP Deficiency rel 1.50

microglia response via both SYK-dependent and SYK-independent pathways

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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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