Systemic Inflammation Brain describes the pathological influence of chronic, low-grade inflammation originating in the periphery on the structure, function, and health of the central nervous system. This peripheral inflammatory state, characterized by elevated circulating cytokines, breaches the blood-brain barrier and activates resident immune cells in the brain, known as microglia. The resulting neuroinflammation is a significant contributor to mood disorders, cognitive decline, and neurodegenerative disease risk.
Origin
This term reflects the growing body of evidence from the fields of neuroimmunology and endocrinology, which has challenged the historical view of the brain as an immune-privileged site. The concept emerged from studies linking elevated C-reactive protein (CRP) and other systemic inflammatory markers to impaired neuroplasticity and altered neurotransmitter metabolism. It highlights the body-wide nature of brain health.
Mechanism
The primary mechanism involves pro-inflammatory cytokines, such as IL-1β and TNF-alpha, crossing the blood-brain barrier or signaling through the vagus nerve. Once inside the brain, these signals activate microglia and astrocytes, initiating a localized inflammatory response. This chronic neuroinflammation impairs the function of neurons and synapses, disrupts the integrity of the neurovascular unit, and ultimately compromises cognitive and emotional regulation.
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