Phenotypic and Functional Plasticity of Glial Cells Under Neuroinflammation: Potential Implications for Brain Repair

Phenotypic and functional plasticity of glial cells under neuroinflammation: potential implications for brain repair

Guest Editor

Senior Research Officer; Adjunct Prof. Jagdeep K. Sandhu

National Research Council Canada, University of Ottawa

[email protected]; [email protected]

Emeritus Researcher Marianna Sikorska-Walker

National Research Council Canada

[email protected]

Message from the Guest Editor

Dear Colleagues,

Astroglia and microglia, are the non-neuronal cells in the mammalian central nervous system (CNS). For a long time glial cells were considered as glue/supporting cells, however it has increasingly become clear that glial cells are active players in brain development and function. Astroglia are the star-shaped cells that are involved in the maintenance of CNS homeostasis by regulating the blood-brain barrier integrity and cerebral blood flow, providing antioxidant and trophic factor support, uptake and recycling of neurotransmitters as well as detoxification of reactive oxygen and nitrogen

species. Astrocytes also provide metabolic support to neurons and regulate short- and long-term

plasticity and memory formation. Microglia are the resident immune cells in the brain parenchyma that play a crucial role in immune surveillance and maintenance of neuronal health. As cellular sensors and effector cells of the CNS, they possess an array of receptors that detect pathological stimuli and are responsible for elimination of the injurious stimuli and restoration of CNS homeostasis. Although earlier studies were focused on the phenotypic alterations of glial cells, newly developed technologies, such as next generation RNA sequencing and spatial transcriptomics have revealed

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heterogeneous populations of ‘homeostatic glia’ and ‘reactive/activated’ glia that has unique ‘molecular signatures’ and perform distinct functions. Glial cells are wired in distinct neural circuits and dysfunction or death of glial cells results in the disruption of these networks, in turn, leading to neuronal cell death. Glial cell dysfunction is associated with an increased production of pathological levels of proinflammatory cytokines and chemokines and development of several age-related neurodegenerative diseases. Taken together, it is evident that both astroglia and microglia are crucial players in supporting neuronal survival and proper functioning of neural circuits and high order brain function. This special issue is dedicated to the plasticity of glial cells under neuroinflammation and possibility to exploit and refocus their function on brain repair mechanisms. We are seeking authors to contribute original research and/or review articles that will discuss how dysfunction of glial cells can result in neuroinflammation, loss of blood-brain (BBB) integrity, failure of neural networks and neuronal cell death. Furthermore, we highly encourage the submission of articles dealing with therapeutic targeting of glia.