Neuroinflammation and Neurodegeneration Mechanisms

This study shows INPP5D expression increases in Alzheimer's disease, particularly in plaque-associated microglia, and suggests it may be a risk factor and therapeutic target.

The paper identifies iron-accumulating microglia in Alzheimer's brains, linking iron uptake to microglial activation and disease pathology.

This study investigates how TREM2 affects the phagocytic, apoptotic, and inflammatory responses to Aβ42 in HMC3 cells, finding TREM2 enhances phagocytosis and inhibits apoptosis and certain inflammatory factors.

This study shows that hyperpolarization of microglia membrane potential is essential for chemotaxis, while depolarization inhibits it.

This study investigates the relationship between age and dystrophic microglia in the human brain, finding that dystrophic microglia are more prevalent in neurodegenerative diseases than in healthy aging.

This study shows that pre-therapeutic microglia activation and sex predict the response to chronic immunomodulation in AD mouse models using TSPO-PET.

This study identifies Alpha B-crystallin as an anti-inflammatory factor secreted by olfactory ensheathing cells that suppresses astrocyte activation and neurotoxicity through exosome-mediated mechanisms.

This study shows that TYROBP-APOE signaling in microglia can occur without TREM2 and influences AD pathology in mouse models.

The paper uses phosphoproteomics to identify Siglec-F and Siglec-8 as upregulated in microglia during neurodegeneration, driving inflammatory responses in mouse and human models.

This study shows that the BMAL1-REV-ERB axis regulates complement expression and microglial synaptic phagocytosis in the hippocampus, with diurnal variation observed in wild-type mice.

The paper profiles microglia transcriptomes in AD donors and non-demented elderly using bulk and single-cell RNA sequencing, finding no significant differences in gene expression or subcluster composition.

The paper introduces a computational model that simulates repair-or-dispose decisions by glia and their long-term implications in neurodegenerative disease progression.

The paper identifies a Csf1r-independent microglial subset in adult mice that exhibits progenitor-like features and is distinct from homeostatic microglia.

This study evaluates IL-34 inhibition as a strategy to reduce microglial proliferation in prion disease, showing tissue-selectivity and reduced side effects compared to CSF1R inhibition.

This study shows that prior hypoxia exposure increases microglial inflammatory gene expression in response to LPS without increasing H3K4me3 at these genes.

This study shows that alcohol intake causes excessive synaptic pruning by microglia, leading to synapse loss and anxiety-like behavior.

This study investigates how TREM2 influences microglial anti-inflammatory responses and shows that reduced TREM2 expression impairs anti-inflammatory gene expression and STAT6 levels.

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 identifies phosphatidylserine (PS) as a neuronal signal that marks synapses for elimination by microglia during development.

This study shows that asperosaponin VI reduces LPS-induced inflammation in microglia by activating the PPAR-gamma pathway.

This paper analyzes juxtavascular microglia dynamics in mice and humans, showing their developmental migration along vessels and stabilization as astrocyte endfeet ensheath the vasculature.

This study shows that 25-HC enhances IL-1β production in microglia, particularly in apoE4-expressing cells, suggesting a role in AD neuroinflammation.

This study shows that activating Fpr2 with QC1 reverses β-amyloid-induced microglial toxicity in vitro by reducing ROS production and metabolic shifts.

This study identifies proteomic changes in microglia during Alzheimer's disease progression in mouse models, showing fibrillar Aβ drives microglial dysfunction.

The paper identifies a novel transcriptional signature in human Alzheimer's myeloid cells that differs from mouse models and shows aging-related and AD-specific gene expression changes.

This study shows that loss of Rhoa in microglia causes neurodegeneration through Src-mediated Tnf production and excitotoxic glutamate secretion.

The paper analyzes RNA-Seq data from young and aged mice after ischemic stroke to identify age-related transcriptional changes and inflammatory responses.

This study identifies a specific GPR56 splicing isoform that mediates microglial synaptic pruning through phosphatidylserine binding, linking it to neurodevelopmental processes.

This study shows that chronic activation of hM3Dq in microglia reduces neuroinflammation and sickness behavior in mice by modulating cytokine responses.