There are various approaches in which one can isolate microglia from murine brains, such as immunomagnetic, density gradient, FACS and differential adhesive methods. In this procedure a modified flask-tapping approach was used due to its simplicity and reproducibility. Our protocol requires only a single step to isolate the microglia from the mixed cell population. Once the microglia were isolated, we characterized cell purity, microglial morphology and phagocytic activity. The single-step protocol, without the need for additional astrocyte or oligodendrocyte separation, allows microglial cells to be used immediately for experimental purposes. The protocol is low-cost and can be performed in any lab with standard cell-culture equipment.
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http://dx.doi.org/10.2144/btn-2022-0054 | DOI Listing |
Eur J Neurol
January 2025
Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine Berlin and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Background: Hyperreflective retinal foci (HRF) visualized by optical coherence tomography (OCT) potentially represent clusters of microglia. We compared HRF frequencies and their association with retinal neurodegeneration between people with clinically isolated syndrome (pwCIS), multiple sclerosis (pwMS), aquaporin 4-IgG positive neuromyelitis optica spectrum disorder (pwNMOSD), and healthy controls (HC)-as well as between eyes with (ONeyes) and without a history of optic neuritis (ONeyes).
Methods: Cross-sectional data of pwCIS, pwMS, and pwNMOSD with previous ON and HC were acquired at Charité-Universitätsmedizin Berlin.
Background: Microglia play a crucial role in clearing amyloid-beta (Aβ) plaques, one of the primary pathological hallmarks of AD. We previously showed that G protein-biased signaling by the G protein-coupled receptor GPR3 reduces soluble Aβ levels and leads to an increase in Aβ plaque compaction and a reduction in Aβ plaque area in the preclinical App AD mouse model. These results suggest a protective microglial response that may limit Aβ plaque formation in G protein-biased GPR3 AD mice.
View Article and Find Full Text PDFBackground: Alzheimer's Disease (AD) is neuropathologically characterized by the accumulation of Amyloid-β (Aβ) plaques, neurofibrillary tangles, and neuroinflammation. GPR3 is a G protein-coupled receptor (GPCR) that has been implicated in Aβ pathogenesis via β-arrestin 2 (βarr2)-mediated intracellular signaling. Genetic deletion of Gpr3 reduces the Aβ plaque burden and cognitive decline in AD transgenic mice.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Anatomy, "Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania.
Neuroimmunology is reshaping the understanding of the central nervous system (CNS), revealing it as an active immune organ rather than an isolated structure. This review delves into the unprecedented discoveries transforming the field, including the emerging roles of microglia, astrocytes, and the blood-brain barrier (BBB) in orchestrating neuroimmune dynamics. Highlighting their dual roles in both repair and disease progression, we uncover how these elements contribute to the intricate pathophysiology of neurodegenerative diseases, cerebrovascular conditions, and CNS tumors.
View Article and Find Full Text PDFExcess lipid droplet (LD) accumulation is associated with several pathological states, including Alzheimer's disease (AD). However, the mechanism(s) by which changes in LD composition and dynamics contribute to pathophysiology of these disorders remains unclear. Apolipoprotein E (ApoE) is a droplet associated protein with a common risk variant (E4) that confers the largest increase in genetic risk for late-onset AD.
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