nevroinflammatorisk

Neuroinflammation, or nevrоinflammatorisk process, refers to the activation of the central nervous system’s innate immune response. It involves glial cells such as microglia and astrocytes, resident CNS immune cells, and, in certain conditions, infiltrating peripheral immune cells. Activation leads to the release of cytokines, chemokines, and other mediators that can help clear pathogens or debris but may also cause tissue damage if prolonged.

Although short-term neuroinflammation can be protective, chronic neuroinflammation is linked to pathology in a range of CNS disorders. Triggers include infections, traumatic injury, stroke, metabolic disturbances, and autoimmune responses. It is also observed in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, where sustained glial activation and inflammatory signaling may contribute to neuronal injury and disease progression. Mechanisms involve microglial activation, astrocytic reactivity, disruption of the blood-brain barrier, and recruitment of peripheral immune cells.

Diagnosis and assessment rely on clinical evaluation, cerebrospinal fluid analysis, neuroimaging, and biomarkers. Imaging techniques such as PET using microglial activation tracers, along with CSF and blood markers of inflammation (for example cytokines and neurodegeneration-related proteins), can indicate ongoing neuroinflammation.

Treatment focuses on addressing the underlying cause and moderating the inflammatory response. This may include antimicrobial therapy for infections, immunomodulatory or immunosuppressive treatments for autoimmune conditions, or supportive care. In research, strategies aim to modulate microglial function, inhibit inflammasomes, or enhance mechanisms that resolve inflammation, with the goal of reducing neural injury while preserving host defense.