Plasticity of microglia in remote regions after focal brain injury. (October 2019)

• Record Type: Journal Article
• Authors: Bisicchia, Elisa; Sasso, Valeria; Molinari, Marco; Viscomi, Maria Teresa
• Is Part Of: Seminars in cell & developmental biology. Volume 94(2019)
• Page Start: 104
• Page End: 111
• Publication Date: 2019-10
• Subjects: DHA docosahexaenoic acid -- EPA eicosapentaenoic acid -- FPR2 formyl peptide receptor 2 -- MPSS Methylprednisolone sodium succinate -- Min minocycline -- Pn pontine nuclei -- RvD1 resolvin D1 -- RvD2 resolvin D2 -- RvE1 resolvin E1 -- SPMs specialized pro-resolving lipid mediators -- TBI traumatic brain injury -- TSPO 18-kDatranslocator protein; Neuroinflammation -- Remote damage -- Microglia -- Specialized pro-resolving lipid mediators -- Brain injury -- Neuroprotection; Cytology -- Periodicals; Developmental biology -- Periodicals; 571.6
• DOI: 10.1016/j.semcdb.2019.01.011
• Languages: English
• ISSNs: 1084-9521

Abstract

Abstract: The CNS is endowed with an intrinsic ability to recover from and adapt secondary compensatory mechanisms to injury. The basis of recovery stems from brain plasticity, defined as the brain's ability to make adaptive changes on structural and functional levels, ranging from molecular, synaptic, and cellular changes in response to alterations in their environment. In this multitude of responses, microglia have an active role and contribute to brain plasticity through their dynamic responses. This review will provide an overview of microglial responses in the context of acute CNS injury and their function in post-traumatic repair and assess the changes that are induced by damage in remote areas from, but functionally connected to, the primary site of injury. In the second section, we highlight the effects of several therapeutic approaches, with particular interest paid to specialized pro-resolving lipid mediators, in modulating microglial responses in remote regions and enhancing long-term functional recovery via suppression of neurodegenerative cascades that are induced by damage, which may contribute to a translational bridge from bench to bedside.