Neuroinflammation Mechanisms encompass the complex cascade of cellular and molecular events within the central nervous system that constitute the brain’s immune response, typically involving the activation of glial cells, release of inflammatory mediators, and recruitment of peripheral immune cells. While acute neuroinflammation is protective, chronic, unresolved low-grade inflammation is a primary driver of neurodegeneration and cognitive dysfunction. Understanding these mechanisms is crucial for therapeutic targeting and preserving neuronal integrity.
Origin
This concept is central to modern neuroscience and neuropathology, linking immune system activity in the brain to the etiology of various neurological and psychiatric disorders. It recognizes the brain’s unique immune environment, distinct from systemic inflammation, and the role of resident cells like microglia and astrocytes. Clinical interventions often focus on modulating this inflammatory environment.
Mechanism
The process is initiated by pathogens, cellular debris, or chronic stress, which activate resident microglia and astrocytes. Activated glial cells release pro-inflammatory cytokines, chemokines, and reactive oxygen species, creating a toxic microenvironment for neurons. Crucially, systemic inflammation, often mediated by hormonal imbalances like high cortisol or insulin resistance, can breach the blood-brain barrier and potentiate these intrinsic neuroinflammatory pathways.
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