What is the Origin of Neural Inflammation?

The term is a compound of "neural," referring to the nervous system, and "inflammation," derived from the Latin inflammare (to set on fire), describing the body's fundamental immune response. The concept emerged from the convergence of neuroscience and immunology, recognizing that the brain is not an "immune privileged" site but rather possesses its own unique, highly regulated immune system. Clinical recognition of chronic neural inflammation is a relatively recent development, linking systemic inflammatory states to central nervous system pathology.

What is the Mechanism of Neural Inflammation?

The core mechanism involves the activation of microglia, the brain's macrophages, which shift from a surveillance state to an active, phagocytic, and cytokine-producing phenotype. Chronic systemic stressors, such as elevated circulating cortisol from HPA axis dysregulation or persistent gut dysbiosis, can trigger this microglial activation via the vagus nerve or by the passage of inflammatory molecules across the blood-brain barrier. Sustained release of pro-inflammatory cytokines, including Interleukin-6 and Tumor Necrosis Factor-alpha, then impairs synaptic plasticity and neuronal communication, leading to functional deficits.

Neural Inflammation

Meaning

Neural Inflammation, often termed neuroinflammation, is the activation of the central nervous system’s resident immune cells, primarily microglia and astrocytes, in response to infection, injury, or chronic systemic stress. This immune response is initially protective, but chronic, unresolved activation leads to the sustained release of pro-inflammatory cytokines, causing damage to neurons and synaptic structures. In the context of hormonal health, neural inflammation can disrupt the delicate balance of neurotransmitters and impair the function of the hypothalamic-pituitary axes, contributing to mood disorders, cognitive decline, and neurodegenerative processes. It is a key factor linking systemic health and brain function.