Topic: Microglia: from homeostasis to neuroinflammation

A special issue of Neuroimmunology and Neuroinflammation

ISSN 2349-6142 (Online), ISSN 2347-8659 (Print)

Submission deadline: 31 Dec 2019

Guest Editor(s)

  • Prof. Isabel Lastres-Becker
    Department of Biochemistry, School of Medicine, Universidad Autónoma de Madrid, Spain.

    Website | E-mail

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 were only relevant to some type of damage, although it has been demonstrated that microglia in a quiescent state has 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 (ROS). Inflammatory factors produced by microglia and astrocytes can damage local brain areas and, can 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 and could contribute to synapse loss and dysfunction, and consequently neurodegenerative disorders.


Microglia, synaptic pruning, inflammation, oxidative stress, phagocytosis, apoptosis, autophagy.

Submission Deadline

31 Dec 2019

Submission Information

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Submission Deadline: 31 Dec 2019
Contacts: Orla Meng, Managing Editor,


Published Articles

This special issue is now open for submission.