neuroinflammatsiooni

Neuroinflammation is inflammation within the central nervous system, encompassing the brain and spinal cord. It is driven by resident immune cells such as microglia and astrocytes and can include infiltration of peripheral immune cells when the blood–brain barrier is compromised. Triggers include infections, traumatic injury, ischemia, toxins, and autoimmune or neurodegenerative processes. While neuroinflammation serves protective roles—clearing pathogens and debris and promoting repair—prolonged or dysregulated responses can contribute to neuronal dysfunction and degeneration.

Cellular and molecular mechanisms involve rapid microglial activation and astrocyte reactivity, and the release of proinflammatory mediators such as TNF-α, IL-1β, and IL-6, as well as chemokines, reactive oxygen species, and nitric oxide. Signaling pathways including NF-κB and inflammasomes (notably NLRP3) participate, and the cascade can disrupt the blood–brain barrier and recruit peripheral leukocytes in certain conditions. The process is dynamic, with acute responses potentially resolving and chronic inflammation correlating with ongoing pathology in various diseases.

In clinical contexts, inflammation participates in both injury and repair. It can exacerbate tissue damage after stroke or traumatic brain injury, yet also support clearance and healing. Chronic neuroinflammation is associated with neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and ALS, though causal relationships are complex and bidirectional.

Diagnosis relies on biomarkers in cerebrospinal fluid or blood and imaging techniques that detect microglial activation, while treatment remains challenging. Corticosteroids are used in specific acute CNS conditions; nonsteroidal anti-inflammatory drugs have limited disease-modifying benefit in most neurodegenerative disorders. Research targets include microglial phenotypes, inflammasome inhibitors, cytokine modulators, and strategies to preserve blood–brain barrier integrity, alongside lifestyle factors that may modulate inflammatory tone.