Abstract: In many tissues, trace metals such as iron (Fe), zinc (Zn), and copper (Cu) are important for various physiological functions such as immune function, cell division, and enzyme function. However, it has been shown in humans and experimental animal models that excessive amounts of these trace metals in the body can induce various diseases in the central nervous system, liver, and respiratory tract. Although the role of zinc in the central nervous system is controversial, with some reports suggesting a protective role, we are interested in the negative effects of excessive amounts of zinc on the central nervous system. Previous studies suggest that zinc, which is released in excessive amounts after ischemic injury, is a major modulator of neuronal death, and that Zn2+-induced neuronal death is an important cause of dementia after ischemic injury (Koh et al., 1996). In addition, other trace metals are present in the brain and/or cerebrospinal fluid, and during neuronal excitation, Cu2+ accumulated in synaptic vesicles is released into the synaptic cleft (Opazo et al., 2014). As the concentrations of these trace metals have been noted to increase, especially under pathological conditions, our research group speculated that these metal-metal interactions may induce neuronal cell death and influence the onset and exacerbation of neurological diseases.