Neuroinflammation is a common feature of diverse nervous system pathologies. In many instances, it begins at an early stage of the disease, paving the way for further exacerbations. The main drivers of neuroinflammation are brain-resident glial cells, such as microglia and astrocytes. Microglia are the primary responders to any insult to the brain parenchyma, translating the signals into diverse molecules. These molecules derived from microglia can regulate the stimuli-dependent reactivity of astrocytes. Once activated, astrocytes in turn, can control microglia phenotypes. Recent evidence indicates that the crosstalk between these glial cells plays an important role in delaying or accelerating neuroinflammation and overall disease progression. To date, various molecules have been recognized as key mediators of the bidirectional communication between microglia and astrocytes. The current review aims to discuss the novel molecules identified recently, which play a critical role in interglial crosstalk, highlighting their therapeutic potential.
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http://dx.doi.org/10.2174/1570159X21666221129121715 | DOI Listing |
Int J Mol Sci
January 2025
Department of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow 117485, Russia.
Traumatic brain injury (TBI) is one of the primary causes of mortality and disability, with arterial blood pressure being an important factor in the clinical management of TBI. Spontaneously hypertensive rats (SHRs), widely used as a model of essential hypertension and vascular dementia, demonstrate dysfunction of the hypothalamic-pituitary-adrenal axis, which may contribute to glucocorticoid-mediated hippocampal damage. The aim of this study was to assess acute post-TBI seizures, delayed mortality, and hippocampal pathology in SHRs and normotensive Sprague Dawley rats (SDRs).
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Methamphetamine is a highly addictive stimulant known to cause neurotoxicity, cognitive deficits, and immune dysregulation in the brain. Despite significant research, the molecular mechanisms driving methamphetamine-induced neurotoxicity and glial cell dysfunction remain poorly understood. This study investigates how methamphetamine disrupts glial cell function and contributes to neurodevelopmental and neurodegenerative processes.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
A.V. Zhirmunsky National Scientific Center of Marine Biology, Far Eastern Branch, Russian Academy of Sciences, 690041 Vladivostok, Russia.
The ultrastructural organization of the nuclei of the tegmental region in juvenile chum salmon () was examined using transmission electron microscopy (TEM). The dorsal tegmental nuclei (DTN), the nucleus of (NFLM), and the nucleus of the oculomotor nerve (NIII) were studied. The ultrastructural examination provided detailed ultrastructural characteristics of neurons forming the tegmental nuclei and showed neuro-glial relationships in them.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS), Universidad Las Palmas de Gran Canaria (ULPGC), Paseo Blas Cabrera Felipe "Físico" 17, 35016 Las Palmas de Gran Canaria, Spain.
In vitro models play a pivotal role in advancing our understanding of neurodegenerative diseases (NDs) such as Parkinson's and Alzheimer's disease (PD and AD). Traditionally, 2D cell cultures have been instrumental in elucidating the cellular mechanisms underlying these diseases. Cultured cells derived from patients or animal models provide valuable insights into the pathological processes at the cellular level.
View Article and Find Full Text PDFBiomolecules
December 2024
Neurochemical Research Unit and Bebensee Schizophrenia Research Unit, Department of Psychiatry and Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB T6G 2G3, Canada.
Schizophrenia is a complex heterogenous disorder thought to be caused by interactions between genetic and environmental factors. The theories developed to explain the etiology of schizophrenia have focused largely on the dysfunction of neurotransmitters such as dopamine, serotonin and glutamate with their receptors, although research in the past several decades has indicated strongly that other factors are also involved and that the role of neuroglial cells in psychotic disorders including schizophrenia should be given more attention. Although glia were originally thought to be present in the brain only to support neurons in a physical, metabolic and nutritional capacity, it has become apparent that these cells have a variety of important physiological roles and that abnormalities in their function may make significant contributions to the symptoms of schizophrenia.
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