Neuroinflammation refers to immune and inflammatory processes within the central nervous system involving microglia, astrocytes, neurons, endothelial cells and infiltrating immune cells. It can be protective in the short term but becomes harmful when chronic or dysregulated.

A key driver of neuroinflammation is activation of pattern recognition receptors such as Toll like receptors by danger signals from pathogens, damaged cells or misfolded proteins. This triggers intracellular cascades involving NF kappa B, MAP kinases and inflammasomes, particularly NLRP3, leading to production of cytokines such as IL 1 beta, IL 6 and TNF alpha, as well as reactive oxygen and nitrogen species.

Microglia adopt distinct activation states ranging from pro inflammatory to pro repair phenotypes. Their balance is influenced by systemic inflammation, aging, metabolic status and the gut microbiome. The blood brain barrier both responds to and shapes inflammatory signaling, with its disruption allowing peripheral immune cells and molecules to enter the brain.

Chronic neuroinflammation contributes to synaptic dysfunction, impaired neurogenesis, oxidative stress, mitochondrial dysfunction and ultimately neurodegeneration. It is strongly implicated in disorders such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, depression and cognitive decline with aging.

Current research targets several intervention points: blocking inflammasome activation, modulating microglial phenotype, restoring blood brain barrier integrity, dampening oxidative stress and altering gut microbiota. Lifestyle factors such as diet, exercise and sleep also influence neuroinflammatory tone. Overall, neuroinflammation is now viewed as a central, dynamic process linking immune status, brain function and neurodegenerative disease.