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作 者:Alexandra M.Barnett Fulton T.Crews Leon G.Coleman
机构地区:[1]Bowles Center for Alcohol Studies,The University of North Carolina at Chapel Hill,School of Medicine,Chapel Hill,NC,USA [2]Department of Pharmacology,The University of North Carolina at Chapel Hill,School of Medicine,Chapel Hill,NC,USA [3]Department of Psychiatry,The University of North Carolina School of Medicine,Chapel Hill,NC,USA
出 处:《Neural Regeneration Research》2021年第6期1204-1205,共2页中国神经再生研究(英文版)
基 金:supported by the National Institutes of Health,National Institute on Alcoholism and Alcohol Abuse(P60AA011605-Fulton Crews,U01AA020023-Fulton Crews,U24AA020024-Fulton Crews,U54AA019767-Fulton Crews,T32AA007573-Fulton Crews;K08AA024829-Leon G Coleman,Jr;K08AA024829S1-Leon G Coleman,Jr,and the Bowles Center for Alcohol Studies).
摘 要:Microglia have multiple functions and phenotypes that can prevent or worsen neuropathology.Microglial depletion and repopulation methods provide a promising technique for understanding microglial biology.Their utility as therapeutic modalities is now under consideration.As resident immune cells in the central nervous system(CNS),microglia maintain the local environment and promote neuronal vitality.However,persistent proinflammatory signaling due to aberrant microglial activation can be detrimental.This is seen in settings such as traumatic brain injury(TBI)(Henry et al.,2020),stroke(Li et al.,2017),and alcohol use disorder(AUD)(Coleman et al.,2020),when the loss of homeostatic control results in persistent proinflammatory signaling that contributes to ongoing neuropathology(Figure 1).Thus,selective replacement of chronically proinflammatory-activated microglia could improve functional outcomes.
分 类 号:R338[医药卫生—人体生理学]
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