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The circadian system is an evolutionarily adaptive system that synchronizes biological and physiological activities within the body to the 24 h oscillations on Earth. At the molecular level, circadian clock proteins are transcriptional factors that regulate the rhythmic expression of genes involved in numerous physiological processes such as sleep, cognition, mood, and immune function. Environmental and genetic disruption of the circadian clock can lead to pathology. For example, global deletion of the circadian clock gene Rev-erbα (RKO) leads to hyperlocomotion, increased anxiety-like behaviors, and cognitive impairments in male mice; however, the mechanisms underlying behavioral changes remain unclear. Here we hypothesized that RKO alters microglia function leading to neuroinflammation and altered mood and cognition, and that microglia depletion can resolve neuroinflammation and restore behavior. We show that microglia depletion (CSF1R inhibitor, PLX5622) in 8-month-old RKO mice ameliorated hyperactivity, memory impairments, and anxiety/risky-like behaviors. RKO mice exhibited striking increases in expression of pro-inflammatory cytokines (e.g., IL-1β and IL-6). Surprisingly, these increases were only fully reversed by microglia depletion in the male but not female RKO hippocampus. In contrast, male RKO mice showed greater alterations in microglial morphology and phagocytic activity than females. In both sexes, microglia depletion reduced microglial branching and decreased CD68 production without altering astrogliosis. Taken together, we show that male and female RKO mice exhibit unique perturbations to the neuroimmune system, but microglia depletion is effective at rescuing aspects of behavioral changes in both sexes. These results demonstrate that microglia are involved in Rev-erbα-mediated changes in behavior and neuroinflammation.
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http://dx.doi.org/10.1016/j.bbi.2023.08.029 | DOI Listing |
Int Immunopharmacol
September 2025
Department of Emergency and Critical Care Medicine, The Second Affiliated Hospital of Soochow University, #1055 Sanxiang Road, Suzhou 215004, Jiangsu, China. Electronic address:
β-Glucan, a polysaccharide from Saccharomyces cerevisiae with immunomodulatory activities that may not trigger pro-inflammatory responses in microglia, has been reported to show rapid antidepressant effects in chronically stressed animals by restoring microglial function in the dentate gyrus. However, the mechanisms underlying this effect of β-glucan are still largely unclear. Considering the importance of astrocytic purinergic 2Y1 receptors (P2Y1Rs) and brain-derived neurotrophic factor (BDNF) in the antidepressant effects of microglial stimulation, we hypothesize that β-glucan produces antidepressant effects by mobilizing astrocytic P2Y1R-triggered BDNF signaling in the hippocampus.
View Article and Find Full Text PDFRedox Biol
August 2025
i3S - Instituto de Investigação e Inovação em Saúde da Universidade do Porto, Porto, Portugal; IBMC - Instituto de Biologia Molecular e Celular, Porto, Portugal; Departamento de Biomedicina - Unidade de Biologia Experimental, Faculdade de Medicina da Universidade do Porto, Porto, Portugal. Elec
Despite clear evidence that vitamin C levels are depleted in the brains of Alzheimer's disease (AD) patients, dietary supplementation has consistently failed in clinical trials, suggesting a critical bottleneck not in systemic supply, but in its transport into brain cells. Here, we identify this bottleneck as a progressive downregulation of the ascorbate transporter, Slc23a2, also known as SVCT2, in microglia. Then we hypothesized that bypassing this cellular deficiency via targeted SVCT2 overexpression in microglia could either prevent the onset of pathology or rescue established functional deficits.
View Article and Find Full Text PDFbioRxiv
August 2025
Department of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA.
Chronic alcohol use is a major modifiable risk factor for Alzheimer's disease (AD), yet the mechanisms by which it modulates AD pathophysiology remain unclear. Here, we examined circuit-level and pathological changes in two distinct AD mouse models, humanized Aβ knock-in (hAPP-KI) (Aβ-driven) and PS19 (tau-driven), subjected to a chronic intermittent alcohol exposure paradigm. In hAPP-KI mice, alcohol increased Aβ accumulation and excitatory transmission in the medial prefrontal cortex (mPFC) while reducing corticostriatal transmission and striatal cholinergic output.
View Article and Find Full Text PDFJ Nanobiotechnology
September 2025
Brain Injury Center, Department of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Microglia play a critical role in neuroinflammation, a key secondary injury mechanism following traumatic brain injury (TBI). The colony-stimulating factor 1 receptor (CSF-1R) inhibitor PLX5622 has shown promise in suppressing neuroinflammation by depleting microglia, but it lacks specificity in targeting microglia at the injury site. To overcome this limitation, we developed PLX5622 nanoparticles functionalized with the CAQK peptide for lesion-specific targeting and combined them with a hydrogel (GelMA-PPS) that possesses potent reactive oxygen species (ROS) scavenging capabilities.
View Article and Find Full Text PDFBrain Sci
July 2025
Department of Brain and Neuroscience, Tokyo Metropolitan Institute of Medical Science, Setagaya 156-8506, Japan.
Murine microglia exhibit rapid self-renewal upon removal from the postnatal brain. However, the signaling pathways that regulate microglial repopulation remain largely unclear. To address this knowledge gap, we depleted microglia from mixed glial cultures using anti-CD11b magnetic particles and cultured them for 4 weeks to monitor their repopulation ability in vitro.
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