Microglia, the innate immune cells of the CNS, are critical for the regulation of the neuronal network, from early neuronal developmental stages to adulthood. They act as brain macrophages, wiping out cell debris and phagocytizing viruses and bacteria. They support the development, maintenance, homeostasis and repair of the brain.
Microglia’s resting state is sensitive to environmental stimuli. Indeed, it has been reported that stress conditions can activate aberrant microglia functioning, leading to the adverse onset of neurodegenerative and psychiatric disorders.
In these recent years, researchers have focused their studies on reporting microglia morphological ultrastructures and molecular states related to health and disease conditions. Reporting microglia heterogeneity has become fundamental to identifying microglia-selectively therapies and uncovering the underlying mechanisms that activate the reparative and regenerative functions of microglia.
Many studies have reported the positive effects of drugs on cognitive aspects in neurodegenerative diseases but addressing and dissecting the functioning of microglia-specific therapeutic compounds could help in understanding and evaluating the predicted off-target effects of drugs.
With this Research Topic, we want to analyze and report novel or already well-characterized compounds as microglia-selective neuro therapies that can alter the resting state of microglia, triggering the neuroinflammation processes. We aim at identifying the molecular action mechanisms of compounds that target (but are not limited to):
- pro-inflammatory microglia (M1 activated state): these microglia secrete proinflammatory cytokines consisting of tumor necrosis factor-a (TNF-a), interleukin (IL)-1ß, IL-6, and iNOS, which lead to dysfunction of the neurotrophic system under conditions of chronic activation;
- neuroprotective microglia (M2 state): drugs preventing microglia activation like inhibitors of K+ channels, blocking of voltage-dependent calcium channels and sodium channels, or modulating the expression of different mediators, such as IL-10 and TGF-ß and pathways related to NRF2 and MAPK signaling.
Microglia, the innate immune cells of the CNS, are critical for the regulation of the neuronal network, from early neuronal developmental stages to adulthood. They act as brain macrophages, wiping out cell debris and phagocytizing viruses and bacteria. They support the development, maintenance, homeostasis and repair of the brain.
Microglia’s resting state is sensitive to environmental stimuli. Indeed, it has been reported that stress conditions can activate aberrant microglia functioning, leading to the adverse onset of neurodegenerative and psychiatric disorders.
In these recent years, researchers have focused their studies on reporting microglia morphological ultrastructures and molecular states related to health and disease conditions. Reporting microglia heterogeneity has become fundamental to identifying microglia-selectively therapies and uncovering the underlying mechanisms that activate the reparative and regenerative functions of microglia.
Many studies have reported the positive effects of drugs on cognitive aspects in neurodegenerative diseases but addressing and dissecting the functioning of microglia-specific therapeutic compounds could help in understanding and evaluating the predicted off-target effects of drugs.
With this Research Topic, we want to analyze and report novel or already well-characterized compounds as microglia-selective neuro therapies that can alter the resting state of microglia, triggering the neuroinflammation processes. We aim at identifying the molecular action mechanisms of compounds that target (but are not limited to):
- pro-inflammatory microglia (M1 activated state): these microglia secrete proinflammatory cytokines consisting of tumor necrosis factor-a (TNF-a), interleukin (IL)-1ß, IL-6, and iNOS, which lead to dysfunction of the neurotrophic system under conditions of chronic activation;
- neuroprotective microglia (M2 state): drugs preventing microglia activation like inhibitors of K+ channels, blocking of voltage-dependent calcium channels and sodium channels, or modulating the expression of different mediators, such as IL-10 and TGF-ß and pathways related to NRF2 and MAPK signaling.
