Inflammation is a complex and coordinated process majorly involved in the innate immune responses to microbial infections and tissue injuries. The complexity of the inflammatory response is observed from different aspects. This includes immune and non-immune cells, which change the microenvironment by producing a plethora of different mediators such as lipid mediators, cytokines and chemokines. These mediators have a central role in all phases of the process. Inflammation in the central nervous system (CNS) plays an important role in neurodegenerative disorders (Parkinson’s and Alzheimer’s diseases). It has been associated with severe inflammatory responses which occur through a variety of cellular and molecular mechanisms, which can include products of oxidative stress.

The current pharmacotherapy mitigating uncontrolled neuroinflammation is mostly anti-inflammatory drugs (steroidal and non-steroidal), immunomodulator agents and biological therapies. However, the continuous use of these agents can reduce efficacy and can potentially have dangerous side effects.

The aim of this Special Issue is to improve our knowledge regarding the cellular and molecular mechanisms of neuroinflammation. We welcome research aiming to improve our understanding of oxidative stress as a pharmacotherapy target mitigating uncontrolled neuroinflammation. Submissions discussing the limitations and advantages of new methods investigating neuroinflammatory responses and oxidative stress are also encouraged. We welcome original research and review articles focusing on either in vitro or in vivo research.

Potential topics include but are not limited to the following:

• Molecular and cellular mechanisms of neuroinflammation
• Oxidative stress as a therapeutic target to mitigate uncontrolled neuroinflammation
• Crosstalk of oxidative stress with others inflammatory mediators in neuroinflammation development
• Antioxidants in neuroinflammation
• New methods investigating neuroinflammatory responses and oxidative stress