This term describes the chronic, low-grade inflammatory state that develops within the central nervous system as an individual ages. It involves the sustained activation of glial cells, particularly microglia and astrocytes, which are the brain’s resident immune cells. This persistent immune response is distinct from acute inflammation and is implicated in neuronal dysfunction and cognitive decline. Understanding this state is crucial for addressing age-related neurological health challenges.
Origin
The concept stems from the convergence of neuroscience, immunology, and gerontology, recognizing that the brain’s immune system undergoes significant changes with age. It is a specific application of the broader ‘inflammaging’ theory to the unique environment of the brain. The ‘neuro’ prefix refers to the nervous system, while ‘inflammation’ denotes the underlying immune response.
Mechanism
The mechanism involves the age-associated failure of microglia to return to a quiescent state after an initial stimulus, leading to a perpetual release of pro-inflammatory cytokines like interleukin-1β and tumor necrosis factor-alpha. This sustained release disrupts the blood-brain barrier integrity and impairs synaptic plasticity. Over time, this chronic immune signaling contributes to oxidative stress and amyloid pathology, creating a hostile environment for neuronal survival and optimal cognitive function.
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