Editorial: Neuroinflammation and Its Resolution: From Molecular Mechanisms to Therapeutic Perspectives

Neuroinflammation, the complex immune response of the central nervous system (CNS), when sustained, is a common denominator in the etiology and course of all major neurological diseases, including neurodevelopmental, neurodegenerative, and psychiatric disorders (e.g., Alzheimer's disease, AD; Parkinson's disease, PD; multiple sclerosis, MS; motor neuron disease; depression; autism spectrum disorder; and schizophrenia).Cellular (microglia and mast cells, two brain-resident immune cells, together with astrocytes) and molecular immune components (e.g., cytokines, complement and patternrecognition receptors) act as key regulators of neuroinflammation (Skaper et al., 2012).In response to pathological triggers or neuronal damage, immune cells start an innate immune response with the aim to eliminate the initial cause of injury.However, when the cellular activity becomes dysregulated, it results in an inappropriate immune response that can be injurious and affect CNS functions.Thus, limiting neuroinflammation and microglia activity represents a potential strategy to alleviate neuroinflammationrelated diseases.The Research Topic collects 20 manuscripts, divided into five sections, that include both original research articles and reviews of the emerging literature and explore the role of neuroinflammation in various neurological diseases.There is particular attention dedicated to the relevant research exploring the mechanisms and mediators involved in the resolution of neuroinflammation.Our aim was to generate a valuable discussion contributing to identify new therapeutic targets in brain damage and providing new drug development opportunities for the prevention and treatment of CNS diseases involving neuroinflammation. PATHOPHYSIOLOGY OF NEUROINFLAMMATIONGuzman-Martinez et al. presented an overview of the various biochemical pathways involved in the neuroinflammatory cascade, focusing on the role of neuroinflammation in the process of protein alteration implicated in various neurodegenerative diseases, such as AD, PD, and Huntington disease.Herradon et al. highlighted the crosstalk between peripheral inflammation and neuroinflammation.The authors described cytokines such as pleiotrophin and midkine as key mediators in modulating both peripheral inflammation and neuroinflammation and they discussed the role of these cytokines in mediating both chronic neuroinflammatory conditions (i.e., neurodegenerative diseases) and peripheral inflammation.Furthermore, the existing therapeutics