Abstract

Zinc, an essential trace element, plays a pivotal role in numerous physiological processes, including immune function, neurotransmission, and antioxidant defense. This review explores zinc’s critical role in maintaining cellular homeostasis and its emerging significance as a therapeutic target in diseases associated with neuroinflammation. Zinc homeostasis involves a complex interplay of absorption, distribution, cellular uptake, and excretion mechanisms regulated by zinc transporters and binding proteins. Moreover, zinc exerts modulatory effects on neuroinflammatory pathways, influencing microglial activation, cytokine production, and oxidative stress responses in the central nervous system. Dysregulation of zinc homeostasis has been implicated in various neuroinflammatory conditions, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Therefore, understanding the mechanisms underlying zinc’s physiological roles and its potential as a therapeutic agent holds promise for developing novel treatments aimed at mitigating neuroinflammation and its associated pathologies. This review synthesizes current research findings to highlight zinc’s dual role as a crucial micronutrient and a promising therapeutic target in neuroinflammatory diseases.