Journal
CELLS
Volume 12, Issue 18, Pages -Publisher
MDPI
DOI: 10.3390/cells12182323
Keywords
prenatal ethanol exposure; microglia; neuroinflammation; extracellular vesicles; neuronal cell death
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This review explores the role of glial cell pathologies, particularly microglia, in fetal alcohol spectrum disorders (FASD). It examines the impact of neuroimmune molecules, signaling pathways, and epigenetic mechanisms on brain function alterations related to FASD. The review also highlights the significance of extracellular vesicles (EVs) in neuron-glia interactions during prenatal alcohol exposure. Potential applications involving nutritional, pharmacological, cell-based, and exosome-based therapies for FASD treatment are discussed.
Fetal alcohol spectrum disorders (FASD) are a set of abnormalities caused by prenatal exposure to ethanol and are characterized by developmental defects in the brain that lead to various overt and non-overt physiological abnormalities. Growing evidence suggests that in utero alcohol exposure induces functional and structural abnormalities in gliogenesis and neuron-glia interactions, suggesting a possible role of glial cell pathologies in the development of FASD. However, the molecular mechanisms of neuron-glia interactions that lead to the development of FASD are not clearly understood. In this review, we discuss glial cell pathologies with a particular emphasis on microglia, primary resident immune cells in the brain. Additionally, we examine the involvement of several neuroimmune molecules released by glial cells, their signaling pathways, and epigenetic mechanisms responsible for FASD-related alteration in brain functions. Growing evidence suggests that extracellular vesicles (EVs) play a crucial role in the communication between cells via transporting bioactive cargo from one cell to the other. This review emphasizes the role of EVs in the context of neuron-glia interactions during prenatal alcohol exposure. Finally, some potential applications involving nutritional, pharmacological, cell-based, and exosome-based therapies in the treatment of FASD are discussed.
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