Oxidative Stress: The Role of Aluminum Ions in Copper Homeostasis Within the Neurons

Aluminum (Al) and copper (Cu) homeostasis is critical for neuronal health. Disruption of their balance contributes to oxidative stress, mitochondrial dysfunction, and neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Existing studies have reported a positive correlation between aluminum and copper concentrations in specific neuronal models. Such homeostatic imbalance may contribute to the activation of pathways related to apoptosis or cuproptosis through mechanisms including oxidative stress, mitochondrial dysfunction, and glutathione depletion. Aluminum-copper dysregulation is considered to potentially play a significant role in certain neurodegenerative disease studies, suggesting that targeted regulation of trace elements may hold potential therapeutic value. However, the specific mechanisms by which maintaining aluminum-copper homeostasis prevents neurodegenerative diseases remain incompletely understood, and further interventional studies focusing on trace elements are urgently needed to validate the causal relationships and clinical application prospects.