Long‐Jun Wu

This study shows TREM2's role in glioblastoma depends on genetic context and timing, with different effects in Nf1-silenced/Ras-driven and PDGFB-driven models.

This study shows that targeting microglial P2Y12 receptor signaling reduces neurodegeneration in Parkinson's disease models using genetic and pharmacological approaches.

The paper identifies astrocyte-to-microglia purinergic signaling as a mechanism converting neuronal hypoactivity into synapse-selective microglial regulation of circuit activity.

This study shows that microglial SWELL1 deficiency increases male-specific seizure severity but protects neurons through impaired phagocytosis and reduced neuroactive metabolite release.

The paper shows that neutrophil-derived C5a signaling through microglial C5aR1 drives reversible motor dysfunction in a mouse NMO model induced by AQP4-IgG.

This study shows that microglia interact with noradrenergic axons in the frontal cortex, enhancing norepinephrine transmission and supporting wakefulness.

This study identifies satellite microglia in adult mice that modulate inhibitory synapses and neuronal activity by physically shielding inhibitory connections.

This study uses brain organoids and assembloids with microglia to show region-specific microglial diversity and their response to SCN2A mutation-induced neuronal hyperactivity.

This study shows that activating microglial Gi signaling reduces microglial activity and disrupts neuronal synchronization.

This study shows DDT exposure increases neuroinflammation in microglia, potentially contributing to Alzheimer's disease risk through direct effects on microglial function.

The paper shows that impaired microglial phagocytosis due to TREM2 deficiency promotes seizure development in mice and correlates with seizure history in human patients.

This study shows human iPSC-derived microglia detect and reduce hyperexcitability in neurons with the SCN2A-L1342P epilepsy mutation through morphological and calcium changes and reduced sodium channel current density.

This study shows that reducing Hv1 proton channels in macrophages improves antigen presentation and anti-tumor responses in glioma by altering macrophage behavior and immune response.

The paper identifies rod-shaped microglia in a TDP-43 mouse model that interact with neuronal dendrites to reduce cortical hyperexcitability and protect against neurodegeneration.

The paper identifies UDP-P2Y6 signaling as a key driver of microglial calcium activity, phagocytosis, and neuroinflammation during epileptogenesis.

The paper shows that higher TREM2 expression in gliomas correlates with poor prognosis, but TREM2 deficiency does not improve outcomes in pre-clinical models, as it impairs myeloid cell phagocytosis and MHCII-dependent CD4+ T cell responses.

This study uses chemogenetic manipulation to show that microglia have both seizure-reducing and seizure-promoting effects in a mouse epilepsy model.

The paper shows ADAM10 regulates macroglial cell fate by promoting astrocyte generation and inhibiting oligodendrocyte production in developing brains.

The paper shows that microglial process dynamics shield GABAergic inputs to enhance neuronal activity after anesthesia in mice.

This study shows that specific MHC class I molecules on brain endothelium regulate CD8 T cell activity and neuropathology in experimental cerebral malaria.

This study shows spinal microglia amplify neuronal activity in inflammatory pain via the P2Y12 receptor, suggesting a therapeutic target for pain management.

This study identifies a novel interaction between TREM2 and TDP-43, showing TREM2 mediates microglial neuroprotection against TDP-43-related neurodegeneration.

This study shows that optogenetic activation of spinal microglia in mice induces chronic pain through IL-1 signaling and increased neuronal activity.

This study uses chemogenetic activation of microglial Gi DREADD to show reduced neuroinflammation and neuropathic pain in mice after spinal nerve injury.

This study shows that blood vessel regression in the brain reduces neuronal activity by impairing mitochondrial metabolism and glutamate production.

This study investigates microglial calcium signaling in vivo, finding that microglial processes respond to changes in neuronal activity through calcium transients, while somatic calcium changes occur only after seizures.

This study shows that neuronal activity in awake mice influences microglial process surveillance via norepinephrine signaling, highlighting the need for awake imaging in studying microglia-neuron interactions.