- Prof. Isabel Lastres-Becker
- Department of Biochemistry, School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain.
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- Dr. Jeffrey Bajramovic
- Alternatives Unit, Biomedical Primate Research Centre, Rijswijk, Netherlands.
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Special Issue Introduction
Microglia are the primary innate immune cells in the CNS, comprising 5–10% of the glial cells in the brain. These cells orchestrate fundamental processes for the development and function of the CNS. For example, microglia are implicated in the regulation of inflammation, apoptosis, phagocytosis of cell debris, synaptic connectivity and synaptic pruning, which are essential aspects for sculpting neural circuits. For a long time, it has been thought that microglia are only relevant to some type of damage, although it has been demonstrated that microglia in a quiescent state have a relevant role in cellular homeostasis and cellular function. On the other hand, microglia play an essential role in the pathophysiology of several neurodegenerative diseases. Microglia are key cellular mediators of neuroinflammatory processes related to the expression of key inflammatory mediators as well as reactive oxygen species. Inflammatory factors produced by microglia and astrocytes can damage local brain areas and, further increase inflammation and glial activation, leading to a vicious inflammatory cycle (chronic neuroinflammation). Here, we review and discuss how those emerging functions that may provide new insight into how disruptions in microglia interact with the microenvironment could contribute to synapse loss and dysfunction, and consequently neurodegenerative disorders.
KeywordsMicroglia, synaptic pruning, inflammation, oxidative stress, phagocytosis, apoptosis, autophagy
Submission Deadline31 Dec 2019