Therapeutic targeting of microglia mediated oxidative stress after neurotrauma

Inflammation is a key part of the body's response to injuries in the central nervous system. Traumatic brain and spinal cord injuries trigger a strong reaction from microglia, brain cells that change shape and produce more reactive oxygen species (ROS). While microglia can initially help with recovery, ongoing inflammation and ROS production can harm other cells. Three major sources of ROS are microglial NADPH oxidase (NOX), mitochondria, and changing iron levels. This review explores existing therapies that target these sources of oxidative stress caused by microglia after an injury, offering suggestions for future research directions.

• 1
  Microglial depletion studies suggest that delayed depletion using PLX5622 reduced microglial ROS and improved outcomes after spinal cord injury, implying that timing is critical for therapeutic efficacy.
• 2
  NOX2 inhibition has been shown to reduce oxidative stress and improve functional recovery after spinal cord injury, highlighting NOX2 as a potential therapeutic target.
• 3
  Therapies targeting mitochondrial ROS have been shown to reduce SCI oxidative stress and improve functional outcomes, further underscoring the importance of mitochondrial health in neurotrauma recovery.