Neuroinflammatory Processes describe the activation of the central nervous system’s resident immune cells, primarily microglia and astrocytes, in response to systemic inflammation, trauma, or chronic metabolic stress. While acute neuroinflammation is protective, chronic, unresolved activation leads to the release of pro-inflammatory cytokines that impair synaptic function, compromise neuronal integrity, and contribute to cognitive decline. Controlling these processes is a critical target in neurological health.
Origin
This term is rooted in immunology and neuroscience, recognizing the brain’s unique immune environment and its intimate connection to peripheral inflammation via the blood-brain barrier and the vagus nerve. The clinical focus arose from evidence linking chronic low-grade systemic inflammation, often driven by hormonal or metabolic dysfunction, to various mood and cognitive disorders. It provides a key mechanism for the mind-body connection.
Mechanism
Systemic inflammatory signals, such as elevated C-reactive protein (CRP) or pro-inflammatory cytokines like interleukin-6, can breach the blood-brain barrier and activate microglia into a sustained pro-inflammatory state. These activated cells release neurotoxic mediators that prune synapses and inhibit neurogenesis in the hippocampus. Modulating hormonal balance, particularly optimizing cortisol and sex steroids, helps to dampen this detrimental immune activation and restore neurotrophic balance.
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