Neuroinflammation and Neurodegeneration Mechanisms

The paper shows that retinal astrocytes undergo large-scale death during development, mediated by microglia rather than apoptosis, leading to anatomical and functional changes in the retinal network.

This study shows TET2 regulates microglial inflammatory responses through NF-κB-dependent pathways and metabolic changes, suggesting it as a target for neurodegenerative diseases.

This study shows NG2 glia are essential for maintaining microglia homeostasis and presents a method to deplete NG2 glia in vitro and in vivo.

This study identifies genetic variants in the MS4A gene cluster associated with higher sTREM2 levels and reduced Alzheimer disease risk, suggesting MS4A4A regulates sTREM2 and contributes to AD pathogenesis.

This study shows that CSF-1 signaling is essential for cerebellar microglia identity and function, and its disruption causes motor and social behavior defects.

This study shows that prenatal inflammation and macrophage depletion affect PV interneuron wiring in two distinct ways during development and adulthood, leading to altered inhibitory circuit function.

This paper introduces two transgenic mouse lines for specific labeling and manipulation of microglia, demonstrating high specificity and minimal off-target effects.

This study shows estrogen promotes microglial pro-resolving behavior and phagocytosis via AnxA1, suggesting potential therapeutic use of selective estrogen receptor ligands for neuroinflammation.

This study shows that sensory lesioning causes microglia to eliminate synapses through ADAM10 and fractalkine signaling, revealing a neuron-to-microglia pathway for synaptic remodeling.

This study develops an organotypic hippocampal slice culture model of neuroinflammation and shows that LPS-induced synaptophysin loss depends on microglia and IL1β.

The paper describes a model of self-limiting acute brain inflammation and identifies gene networks associated with inflammation resolution.

This study shows that microglial SIRPα suppresses the emergence of CD11c+ microglia, which are involved in white matter repair after demyelination.

The paper defines a core transcriptional signature of human microglia through meta-analysis and shows its utility in identifying region-specific alterations in Alzheimer’s disease.

This study shows that adult microglia self-renew to restore homeostasis after ablation, with specific maturation programs and spatial organization.

The paper examines microglial activation in elderly brains, finding strong associations with neuropathology and cognitive decline, and identifies genetic overlaps with Alzheimer's disease.

This study shows that subchronic immune challenges cause sex-specific memory impairments in males and females that persist for months after the challenge.

The paper uses a CRISPR/Cas9 screen in zebrafish to identify Il34 as a factor facilitating yolk sac macrophage distribution and brain colonization.

This study uses scRNA-seq to analyze microglia and myeloid cells across brain regions and developmental stages, revealing heterogeneity in postnatal microglia and their roles in disease.

This paper presents the first 3D ultrastructural reconstruction of an entire mouse hippocampal microglia using SBEM and CLEM, providing a reference for microglia cell biology.

This study identifies nine distinct microglial states in mice across lifespan and after injury using single-cell RNA sequencing, revealing persistent and age-related changes.

This paper compares ischemic inflammation in the heart and brain, finding a second inflammatory wave in the brain post-stroke linked to cholesterol crystals and osteopontin, which drives secondary neurodegeneration.

This paper identifies a neuroprotective subpopulation of monocytes induced by lipopolysaccharide preconditioning that reduces brain injury after stroke in mice.

This study shows that systemic inflammation causes acute cognitive dysfunction and brain injury through separate IL-1-dependent mechanisms, with implications for managing cognitive decline during illness.

This study examines the transcriptional effects of Trem2 loss in mouse brain, revealing disruptions in cell co-expression networks and highlighting a potential role for Trem2 in endothelial cell homeostasis.

The paper identifies a genetic variant near CXCR4 associated with increased risk for PSP and PD, showing dysregulation of CXCR4 and microglia-related genes in neurodegenerative diseases.

This study identifies microglia-mediated synaptic remodeling through trogocytosis and filopodia induction in developing hippocampal cultures.

This study identifies neuronal CCL2 expression as critical for recruiting inflammatory monocytes into the brain during acute TMEV infection.

This study shows that soluble CD163 from activated monocytes suppresses lymphocytes after ischemic stroke, linking innate immune activation to adaptive immune suppression.

This study shows that 7nAChR agonists reverse LPS-induced pro-inflammatory microglial phenotype in fetal sheep, while antagonists enhance it, suggesting therapeutic potential for neuroinflammation.