The clinically observed phenomenon where chronic, low-grade inflammation throughout the body negatively affects central nervous system function, leading to measurable impairments in cognitive domains such as memory, attention, and executive function. This impact is mediated by the passage of pro-inflammatory cytokines and immune cells across the blood-brain barrier. Recognizing this systemic link is essential for treating cognitive decline and mood disorders.
Origin
This concept stems from the field of psychoneuroimmunology, which formally links the immune system and the brain. Research demonstrating that elevated peripheral inflammatory markers, such as C-reactive protein, correlate with cognitive dysfunction solidified this connection. In hormonal health, the origin is linked to the recognition that endocrine imbalances, like insulin resistance or low sex steroids, often drive this chronic systemic inflammation.
Mechanism
The mechanism involves pro-inflammatory cytokines, such as Interleukin-6 and TNF-alpha, crossing the blood-brain barrier where they activate resident immune cells (microglia) and astrocytes. This neuroinflammation disrupts synaptic plasticity, impairs long-term potentiation, and interferes with neurotransmitter metabolism, ultimately damaging neuronal networks critical for cognitive processes. Reducing systemic inflammatory load is therefore a direct strategy for neuroprotection and cognitive support.
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