The illicit use of methamphetamine has been a rising concern in the United States since the turn of the century. There is a well-established association between methamphetamine intoxication and neurodegeneration. Many studies have suggested that the death of neurons is in part contributed to an overzealous response of the immune system following methamphetamine exposure. The immune system utilizes a variety of compounds to carry out its functions, including the naturally found element, zinc. Conversely, excessive buildup of zinc in the brain has been implicated in many neurodegenerative diseases. Similar to the damage that occurs following methamphetamine exposure, neurons are the primary cells that are impaired in these terminal illnesses. Therefore, we hypothesize that accumulation of zinc in the brain could be resulting in neurodegeneration following methamphetamine intoxication. Briefly, mice were injected intraperitoneally with either sterile saline (n=6) or 5 mg/kg methamphetamine (n=6) for ten days. On Day 10, the prefrontal cortex, midbrain, and striatum were isolated and sonicated. Levels of zinc were determined by Total Reflection X-Ray Fluorescence. Zinc levels were significantly increased in the midbrain of animals treated with methamphetamine compared to animals treated with saline (p0.05). These findings can translate into a clinical setting to prevent substantial brain damage following methamphetamine intoxication or overdose in the community. Furthermore, if zinc proves to be a mediator of the immune system and thereby compromises neuron integrity, zinc could serve as a potential biomarker for terminal illnesses that target the brain, including Parkinson’s disease and Alzheimer’s disease.
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