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Neuroinflammation inhibition is a therapeutic strategy and biological process rather than a single molecular target. It involves the modulation of inflammatory responses within the central nervous system (CNS), primarily driven by the innate immune cells of the brain, such as microglia and astrocytes [1][3]. While acute neuroinflammation serves as a defense mechanism against injury or infection, chronic neuroinflammation is a pathological hallmark of various neurodegenerative diseases, including Alzheimer's and Parkinson's, where it exacerbates neuronal loss and cognitive decline [2][4]. Drugs that achieve neuroinflammation inhibition typically act on specific underlying targets like cytokines, kinases, or cell-surface receptors to dampen the release of neurotoxic mediators and oxidative stress [3]. Because the immune system also plays a role in debris clearance and tissue repair, therapeutic approaches must carefully balance the suppression of harmful inflammation with the preservation of neuroprotective functions [4]. Consequently, neuroinflammation inhibition represents a broad pharmacological goal aimed at slowing disease progression and protecting neuronal integrity.
Neuroinflammation inhibition is achieved by suppressing the activation of microglia and astrocytes, reducing the production of pro-inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6), inhibiting the NF-κB and NLRP3 inflammasome pathways, and limiting the infiltration of peripheral immune cells across the blood-brain barrier [1][2].
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