Neurotoxic Metals and Metal Homeostasis in the Brain

Abstract

Cerebral metal homeostasis is essential for neurophysiology. The disruption is produced by dysregulation of critical metals or neurotoxicity from the environment. This chapter compares essential elements such as iron, copper, zinc, and manganese, which play roles in oxidative metabolism, neurotransmission, and myelination, to toxic heavy metals such as lead, mercury, cadmium, and arsenic, which impede these functions. Several regulatory mechanisms are considered, including metal ion transit through the blood-brain barrier, cell chaperoning, storage, and exporting. This chapter also focuses on pathogenic pathways such as oxidative stress, mitochondrial dysfunction, neuroinflammation, and protein misfolding, while also taking into consideration age-related changes. Current therapeutic strategies such as; chelation, modulation of metal-protein interactions, and transport interference are critically evaluated regarding their limitations. Overall, effective neuroprotection demands a multifaceted strategy combining reduced exposure with restored metal homeostasis.