Neuroinflammation refers to immune responses within the brain and spinal cord, primarily involving microglia and astrocytes. Under normal conditions, these cells support neurons, clear debris and maintain homeostasis. When triggered by infection, injury, toxins, metabolic stress or protein aggregates, they can adopt reactive states that are protective at first but damaging if prolonged.

Modern research shows that chronic, low grade neuroinflammation contributes to a wide range of neurological and psychiatric disorders. In Alzheimer’s disease, inflammatory signaling interacts with amyloid beta and tau pathology, shaping disease onset and progression. Genome wide studies have identified immune related risk genes, while imaging and fluid biomarkers reveal glial activation and inflammatory mediators in living patients.

In Parkinson’s disease, activated microglia surround degenerating dopaminergic neurons and release cytokines and reactive oxygen species. Experimental models indicate that inflammation can exacerbate alpha synuclein aggregation and neuronal loss. In multiple sclerosis, immune cells attack myelin, and both peripheral immune infiltration and resident glial responses are central to lesion formation and repair.

Beyond classic neurodegeneration, altered neuroimmune signaling is implicated in depression, schizophrenia and autism spectrum conditions, where it may affect synaptic pruning, connectivity and neurotransmission. Systemic inflammation, aging and metabolic disorders appear to prime microglia, lowering the threshold for harmful responses.

Therapeutic strategies now under investigation include targeting specific cytokines, modulating microglial states, influencing the gut brain immune axis and using lifestyle or metabolic interventions to reduce inflammatory tone. A major challenge is to dampen harmful chronic inflammation while preserving essential immune defense and repair functions.