Neuroinflammation and Neurodegeneration Mechanisms

This study shows Phf15 represses pro-inflammatory genes and antiviral responses in microglia, regulating inflammation during aging and LPS stimulation.

This study shows HERV-K(HML-2) RNA activates TLR8 and Tlr7, causing neurodegeneration in mice and correlating with AD in humans.

This paper identifies distinct cellular mechanisms by which TLR4 regulates network excitability and working memory after brain injury, showing TNF's role in mediating these effects.

This study xenotransplants human PSC-derived microglia into mice to create a chimeric brain model that retains human microglial identity and exhibits disease-relevant responses.

The paper analyzes single-cell RNA profiles from the mouse dorsal raphe nucleus to study antiviral neuroinflammatory responses following rabies virus infection, identifying distinct immune cell populations and microglia states.

This study identifies a novel neuroprotective mechanism where microglia clear neuron-released α-synuclein via TLR4-NF-κB-p62 mediated selective autophagy, preventing neurodegeneration.

This study shows that human iPSC-derived astrocytes exposed to TNF-alpha recapitulate key astrogliosis features over time, including cytokine secretion, morphological changes, and reduced aspartate uptake.

The paper identifies lipid droplet-accumulating microglia (LAM) as a dysfunctional, pro-inflammatory state in aging brains, linked to neurodegeneration.

This study identifies enduring and sex-specific changes in hippocampal gene expression following a subchronic immune challenge, with males showing persistent dysregulation while females exhibit differential responses to subsequent challenges.

This study uses scRNA-seq to compare microglia in adult mouse brains and spinal cords, identifying subtype differences and plasticity in response to HIV-1 gp120.

The paper uses scRNA-seq to show genetic variation in microglia from different mouse strains affects their heterogeneity and response to amyloidosis in Alzheimer's disease models.

This study examines the relationship between microglial activation and white matter changes in dementia with Lewy bodies using PET and DTI imaging.

This study shows that csf1rb is essential for adult microglia development in zebrafish, while csf1ra is involved in embryonic microglia.

This study shows that pharmacological depletion of microglia prevents short-term memory impairment in Ang II-induced hypertension.

This study identifies synapse loss and microglial synaptic engulfment in MS models and demonstrates that targeted complement inhibition prevents synapse loss and visual dysfunction.

This study shows that reducing CSF-2 in Csf1r+/- mice rescues behavioral and histopathological deficits in ALSP by preventing microgliosis and transcriptomic changes, suggesting CSF-2 as a therapeutic target.

This study shows that TREM2 loss-of-function variants in human iPSC-derived microglia impair metabolic switching and PPARγ/p38MAPK signaling, affecting β-Amyloid phagocytosis.

The paper identifies specialized somatic microglia-neuron junctions that enable microglia to monitor and protect neuronal function through purinergic signaling.

This study identifies DDX3 inhibition as a potential therapy for HAND by blocking Tat and cocaine-induced microglial activation and neurotoxicity in rat and mouse models.

This study shows that microglia in zebrafish tauopathy models become more mobile and change morphology, and their ablation increases Tau hyperphosphorylation.

This study shows microglia control vessel calcification via TREM2, with ablation worsening calcification and revealing a new role in preventing ectopic calcification.

This study shows that URMC-099 prevents surgery-induced microglial activation and cognitive decline in a mouse model of PND without affecting bone healing.

The paper demonstrates that human microglia derived from embryonic stem cells can engraft mouse brains and express Alzheimer's risk genes when exposed to Aβ, offering a new model to study genetic risk in AD.

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.

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.