neuroinflammation

Neuroinflammation is the central nervous system's immune response to injury, infection, or disease, involving glial activation, inflammatory mediators, and vascular changes. It encompasses local changes within the brain and spinal cord and, at times, involvement of the peripheral immune system.

The main resident immune cells are microglia, which survey the CNS environment and respond to disturbances. Astrocytes also participate in immune signaling and in forming scar tissue after injury. Upon activation, these cells release a range of inflammatory mediators, including cytokines such as interleukin-1 beta, interleukin-6, and tumor necrosis factor alpha, chemokines, prostaglandins, and reactive oxygen species. The blood-brain barrier can become permeable during neuroinflammation, allowing peripheral immune cells such as monocytes and T cells to enter the CNS.

Neuroinflammation can be acute and protective, helping to clear pathogens and damaged debris. However, when it becomes chronic, sustained mediator production can contribute to neuronal dysfunction and tissue damage, potentially driving or exacerbating neurodegenerative and neuropsychiatric conditions.

Neuroinflammation is linked to a range of disorders, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, stroke, and traumatic brain injury. Biomarkers such as cytokines in cerebrospinal fluid or blood, neurofilament light chain, and imaging indicators of microglial activation (for example, PET tracers targeting microglia) are used in research and clinical contexts. Therapeutic approaches seek to modulate inflammatory responses, including cytokine inhibition, microglial-targeted therapies, and modulation of the complement system, though achieving a balance between protective and harmful effects remains a key challenge.