Neuroinflammation, the complex immune response of the central nervous system (CNS), if sustained, is a common denominator in the etiology and course of all major neurological diseases, including neurodevelopmental, neurodegenerative and psychiatric disorders (e.g., Alzheimer disease, Parkinson disease, multiple sclerosis, motor neuron disease, depression, autism spectrum disorder and schizophrenia). Cellular and molecular immune components such as microglia and astrocytes, cytokines, complement and pattern-recognition receptors act as key regulators of neuroinflammation. Their dysregulated activity during embryonic, early post-natal or adult life results in an inappropriate immune response that can be injurious and affect CNS functions. The exact mechanisms underlying the link between neuroinflammation and CNS disorders are still not clear and the study of innovative pharmacological approaches targeting neuroinflammation and its resolution is currently an emerging field of research. Traditionally, research has focused on developing anti-inflammatory drugs to modulate the pro- or anti-inflammatory profile of the inflammatory process. More recently, the identification of mechanisms and mediators involved in the resolution of neuroinflammation is of growing interest.
In this Research Topic, which will comprise both original research articles (in vitro, animal or clinical studies) and reviews, we invite researchers to discuss the key cellular and molecular mechanisms activated by CNS immune cells in response to injurious stimuli, with a particular attention dedicated to the recent evidence exploring the mechanisms and mediators involved in the resolution of neuroinflammation. A better understanding of these mechanisms may contribute to identify new therapeutic targets in brain damage and provide new drug development opportunities (i.e., “pro-resolving agents”) for the prevention and treatment of CNS diseases involving neuroinflammation.
Neuroinflammation, the complex immune response of the central nervous system (CNS), if sustained, is a common denominator in the etiology and course of all major neurological diseases, including neurodevelopmental, neurodegenerative and psychiatric disorders (e.g., Alzheimer disease, Parkinson disease, multiple sclerosis, motor neuron disease, depression, autism spectrum disorder and schizophrenia). Cellular and molecular immune components such as microglia and astrocytes, cytokines, complement and pattern-recognition receptors act as key regulators of neuroinflammation. Their dysregulated activity during embryonic, early post-natal or adult life results in an inappropriate immune response that can be injurious and affect CNS functions. The exact mechanisms underlying the link between neuroinflammation and CNS disorders are still not clear and the study of innovative pharmacological approaches targeting neuroinflammation and its resolution is currently an emerging field of research. Traditionally, research has focused on developing anti-inflammatory drugs to modulate the pro- or anti-inflammatory profile of the inflammatory process. More recently, the identification of mechanisms and mediators involved in the resolution of neuroinflammation is of growing interest.
In this Research Topic, which will comprise both original research articles (in vitro, animal or clinical studies) and reviews, we invite researchers to discuss the key cellular and molecular mechanisms activated by CNS immune cells in response to injurious stimuli, with a particular attention dedicated to the recent evidence exploring the mechanisms and mediators involved in the resolution of neuroinflammation. A better understanding of these mechanisms may contribute to identify new therapeutic targets in brain damage and provide new drug development opportunities (i.e., “pro-resolving agents”) for the prevention and treatment of CNS diseases involving neuroinflammation.