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Granular cytoplasmic inclusions in astrocytes and microglial activation in the fetal brain of pigtail macaques in response to maternal viral infection.
Acta Neuropathol Commun
March 2025
Department of Obstetrics and Gynecology, University of Washington, Seattle, WA, USA.
The fetal origins of neuropsychiatric disorders are poorly understood but have been linked to viral or inflammatory injury of the developing brain. The fetal white matter is particularly susceptible to injury as myelination, axonal growth, and deep white matter tracts become established. We have used the pigtail macaque (Macaca nemestrina) to study the maternal and fetal effects of influenza A virus (FLUAV) and Zika virus (ZIKV) infection during pregnancy, in cohorts with different time intervals between inoculation and delivery.
View Article and Find Full Text PDFA versatile mouse model to advance human microglia transplantation research in neurodegenerative diseases.
Mol Neurodegener
March 2025
VIB Center for Brain and Disease Research and Department of Neurosciences, KU Leuven, Louvain, Belgium.
Background: Recent studies highlight the critical role of microglia in neurodegenerative disorders, and emphasize the need for humanized models to accurately study microglial responses. Human-mouse microglia xenotransplantation models are a valuable platform for functional studies and for testing therapeutic approaches, yet currently those models are only available for academic research. This hampers their implementation for the development and testing of medication that targets human microglia.
View Article and Find Full Text PDFTargeting brain macrophages: NF-κB as a therapeutic gateway in melanoma brain metastasis.
Cancer Cell
March 2025
Washington University in St. Louis, Saint Louis, MO, USA. Electronic address:
Melanoma brain metastasis (MBM) is associated with poor prognosis. In this issue of Cancer Cell, Rodriguez-Baena et al. identify nuclear factor κB (NF-κB) (Rela) as a driver of pro-tumoral microglia in MBM.
View Article and Find Full Text PDFLuteolin attenuates cadmium neurotoxicity by suppressing glial inflammation and supporting neuronal survival.
Int Immunopharmacol
March 2025
Key Laboratory of Ecology and Environment in Minority Areas National Ethnic Affairs Commission, Center on Translational Neuroscience, College of Life and Environmental Sciences, Minzu University of China, Beijing 100081, China.. Electronic address:
Cadmium (Cd), a neurotoxic metal, is associated with the development of neurological disorders. This study investigated the neuroprotective effects of Luteolin against Cd-induced toxicity in cultured cells and mouse models. Our findings demonstrate that Luteolin protects hippocampal neurons from Cd toxicity and mitigates Cd-triggered inflammatory responses in microglial BV2 cells.
View Article and Find Full Text PDFImplications for soluble iron accumulation, oxidative stress, and glial glutamate release in motor neuron death associated with sporadic amyotrophic lateral sclerosis.
Neuropathology
March 2025
Department of Pathology, Tokyo Women's Medical University, Tokyo, Japan.
Oxidative stress in sporadic amyotrophic lateral sclerosis (ALS) has been evidenced by accumulation of oxidatively modified products of nucleic acids, lipids, sugars, and proteins in the motor neuron system of brains and spinal cords obtained at autopsy from the patients. We recently demonstrated soluble iron accumulation in activated microglia of sporadic ALS spinal cords. This finding could indicate that iron-mediated Fenton reaction is most likely to be responsible for oxidative stress associated with this disease.
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