Neuroinflammation and Neurodegeneration Mechanisms

Pre-therapeutic Microglia Activation and Sex Determine Therapy Effects of Chronic Immunomodulation

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

Molecular and functional properties of PFC astrocytes during neuroinflammation-induced anhedonia

This study examines how neuroinflammation affects astrocyte gene expression in the mouse medial prefrontal cortex and links these changes to anhedonia, finding shared pathways with human major depressive disorder and Alzheimer's disease.

Cortical stroke produces secondary injury and long-lasting gliosis in the ipsilateral thalamus

This study shows that cortical stroke causes long-lasting gliosis in the ipsilateral thalamus, with memantine reducing gliosis at 2 weeks post-stroke.

A Novel Factor in Olfactory Ensheathing Cell-Astrocyte Crosstalk: Anti-Inflammatory Protein α- Crystallin B

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.

Reactive or transgenic increase in microglial TYROBP reveals a TREM2-independent TYROBP-APOE link in wild-type and Alzheimer's-related mice

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

Microglia orchestrate neuronal activity in brain organoids

This study shows that incorporating microglial progenitors into human brain organoids supports neuronal maturation and synaptic activity.

Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration

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.

REV-ERBalpha mediates complement expression and circadian regulation of microglial synaptic phagocytosis

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.

Profiling microglia from AD donors and non-demented elderly in acute human post-mortem cortical tissue

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.

How repair-or-dispose decisions under stress can initiate disease progression

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

Neural inflammation alters synaptic plasticity probed by 10 Hz repetitive magnetic stimulation

The paper investigates how systemic inflammation affects synaptic plasticity using repetitive magnetic stimulation and shows that anti-inflammatory cytokines can restore plasticity in inflamed tissue cultures.

A Mac2-positive progenitor-like microglial population survives independent of CSF1R signaling in adult mouse brain

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

Inhibition of IL34 unveils tissue-selectivity and is sufficient to reduce microglial proliferation in chronic neurodegeneration

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.

Microglia Stimulate Zebrafish Brain Repair Via a Specific Inflammatory Cascade

This study shows that microglia promote zebrafish brain repair through specific inflammatory signaling pathways, highlighting their role in neurogenesis and inflammation resolution.

Prior hypoxia exposure enhances murine microglial inflammatory gene expression in vitro without concomitant H3K4me3 enrichment

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

Neuroinflammation characterizes the earliest changes in Alzheimer's disease pathology and associated subjective cognitive impairment in adult hydrocephalus biopsies

The paper identifies gene expression changes in Alzheimer's disease pathology linked to cognitive impairment in hydrocephalus biopsies, showing microglial activation and loss of homeostatic genes.

Alcohol intake triggers aberrant synaptic pruning leading to synapse loss and anxiety-like behavior

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

Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions

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

Chronic Intermittent Ethanol Activates CHOP in Striatal Microglia and Exacerbates Ethanol Withdrawal

This study investigates how chronic intermittent ethanol affects microglial translatome in striatum, identifying CHOP and UPR as key factors in ethanol withdrawal symptoms.

Innate immune signaling and sex differences contribute to neurocognitive impairment, neuroinflammation, and mitochondrial rewiring in a mouse model of Gulf War illness

This study shows that GWIC exposure affects mitochondrial function and innate immune signaling in mice, leading to neurocognitive impairments and sex-specific differences.

TREM2 R47H exacerbates immune response in Alzheimer's disease brain

This study investigates how the TREM2 R47H variant affects immune responses in Alzheimer's disease by comparing gene expression in different patient groups.

Microglial Calcium Signaling is Attuned to Neuronal Activity

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.

Systemic inflammation causes microglial dysfunction with a mixed AD-like pathology.

This study shows that chronic systemic inflammation in mice leads to brain changes resembling mixed vascular and Alzheimer's disease pathology, including tauopathy and microglial dysfunction.

AD-linked R47H-TREM2 mutation induces disease-enhancing proinflammatory microglial states in mice and humans

This study identifies R47H-TREM2 mutation-induced proinflammatory microglial states in human AD and tauopathy mice, showing Akt pathway involvement and potential therapeutic targets.

Masitinib mediates TGF-Beta1 and Nitric Oxide Secretion and Ameliorates MPTP/Microglia-Induced Degeneration of Differentiated SH-SY5Y Cells

Local externalization of phosphatidylserine mediates developmental synaptic pruning by microglia

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

Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-gamma pathway in primary microglia

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

A developmental analysis of juxtavascular microglia dynamics and interactions with the vasculature

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

Activation of the pro-resolving receptors Fpr2/3 attenuate lipopolysaccharide-induced inflammatory microglial activation

This study shows that activating Fpr2/3 receptors reduces LPS-induced inflammation in microglia by inhibiting NFκB and promoting resolution.

25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner

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