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Glial cells serve as fundamental regulators of the central nervous system in development, homeostasis, and disease. Discoveries into the function of these cells have fueled excitement in glial research, with enthusiastic researchers addressing fundamental questions about glial biology and producing new scientific tools for the community. Here, we outline the pros and cons of in vivo and in vitro techniques to study astrocytes and microglia with the goal of helping researchers quickly identify the best approach for a given research question in the context of glial biology. It is truly a great time to be a glial biologist.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6314517 | PMC |
http://dx.doi.org/10.1084/jem.20180200 | DOI Listing |
Exp Neurol
September 2025
CNRS UMR 5536 RMSB, University of Bordeaux, Bordeaux, France; Basic Science Department, Loma Linda University School of Medicine, Loma Linda, CA, USA; CNRS UMR 7372 CEBC, La Rochelle University, Villiers-en-Bois, France.
Introduction: The vulnerability of white matter (WM) in acute and chronic moderate-severe traumatic brain injury (TBI) has been established. In concussion syndromes, including preclinical rodent models, lacking are comprehensive longitudinal studies spanning the mouse lifespan. We previously reported early WM modifications using clinically relevant neuroimaging and histological measures in a model of juvenile concussion at one month post injury (mpi) who then exhibited cognitive deficits at 12mpi.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Department of Pharmacology, Govt. College of Pharmacy, Rohru, Shimla, Himachal Pradesh, 171207, India.
Alzheimer's disease (AD) is the most common, complex, and untreatable form of dementia which is characterized by severe cognitive, motor, neuropsychiatric, and behavioural impairments. These symptoms severely reduce the quality of life for patients and impose a significant burden on caregivers. The existing therapies offer only symptomatic relief without addressing the underlying silent pathological progression.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Department of Anesthesiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 XianXia Road, Shanghai 200336, China; Hongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 XianXia Road, Shanghai 200336, China. El
Hypoxic-ischemic brain damage (HIBD) is a severe condition leading to extensive neuronal loss and functional impairments, representing a significant challenge in neonatal care. PFGA12, a peptide derived from fibrinogen alpha chain (FGA), which is notably downregulated in the umbilical cord blood of hypoxic-ischemic encephalopathy (HIE) infants. We demonstrate that PFGA12 significantly enhances cell viability and mitigates oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuronal cell death.
View Article and Find Full Text PDFNeurochem Res
September 2025
International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
The concept of the central nervous system (CNS) reserve emerged from the mismatch often observed between the extent of brain pathology and its clinical manifestations. The cognitive reserve reflects an "active" capacity, driven by the plasticity of CNS cellular components and shaped by experience, learning, and memory processes that increase resilience. We propose that neuroglial cells are central to defining this resilience and cognitive reserve.
View Article and Find Full Text PDFBrain
September 2025
Central European Institute of Technology Masaryk University (CEITEC MU), 625 00 Brno, Czech Republic.
Mutations in the human ADAR gene encoding adenosine deaminase acting on RNA 1 (ADAR1) cause Aicardi-Goutières syndrome 6 (AGS6); a severe auto-inflammatory encephalopathy with aberrant interferon (IFN) induction. AdarΔ2-13 null mutant mouse embryos lacking ADAR1 protein die with high levels of IFN-stimulated gene (ISG) transcripts. In Adar Mavs double mutants also lacking the Mitochondrial antiviral signaling (MAVS) adaptor, the aberrant IFN induction is prevented.
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