Neuroinflammation, Immune Crosstalk & CNS Immunotherapeutics
Neuroinflammation is increasingly recognized as a key driver in the onset and progression of CNS disorders, emerging from complex interactions between neurons, glial cells, and peripheral immune systems. Dysregulated microglial activation, cytokine storms, and chronic inflammatory cycles can accelerate neurodegeneration and impair neural repair. Understanding the mechanisms of immune crosstalk such as blood–brain barrier permeability changes, peripheral immune infiltration, and maladaptive complement activation has opened pathways for targeted immunotherapeutic strategies. Novel treatments aim to modulate neuroinflammatory cascades, reprogram microglial activity, block damaging cytokines, and enhance protective immune pathways. Immunotherapeutics, including monoclonal antibodies, small-molecule inhibitors, RNA-targeted therapies, and nanocarriers, offer precision modulation of inflammatory mediators. These approaches are reshaping therapies for multiple sclerosis, Alzheimer’s disease, autoimmune encephalitis, neuropathic pain, and traumatic brain injury. By targeting both acute and chronic inflammatory processes, next-generation interventions aim to slow disease progression, protect neuronal function, and promote long-term neurological recovery.
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