Neuro-Inflammation Signals refer to the complex array of biochemical messengers, including pro-inflammatory cytokines and chemokines, that are released by activated glial cells within the central nervous system. These signals indicate an immune response within the brain and spinal cord, often triggered by systemic inflammation, trauma, or chronic stress. Sustained neuro-inflammation can disrupt the delicate balance of neurotransmitter function and compromise the integrity of the blood-brain barrier. Clinically, these signals are strongly implicated in mood disorders, cognitive decline, and the dysregulation of the neuroendocrine axes.
Origin
The term emerged from the convergence of neuroscience and immunology, recognizing that the brain, once thought to be immune-privileged, possesses its own resident immune system composed of microglia and astrocytes. Research solidified the understanding that these cells actively participate in pathology, generating inflammatory signals that profoundly affect neuronal function. This concept is central to modern psychoneuroimmunology.
Mechanism
When activated by a peripheral inflammatory stimulus or direct neural insult, glial cells shift from a surveillance state to an active, pro-inflammatory phenotype, releasing signaling molecules like Interleukin-1 beta (IL-1β) and Tumor Necrosis Factor-alpha (TNF-α). These signals interfere with synaptic plasticity and neuronal communication, often leading to oxidative stress and excitotoxicity. Furthermore, they can directly modulate the hypothalamic-pituitary-adrenal (HPA) axis, linking brain inflammation to systemic hormonal stress responses.
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