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
