We studied 10 patients with Minamata disease (organic mercury poisoning) who have been followed for over 20 years. CT revealed a bilateral, symmetric, low-density area in the visual cortex and diffuse atrophy of the cerebellar hemispheres and vermis, especially the inferior vermis. Computerized quantitative analysis of the tremor of these patients showed a peculiar frequency of 7.075 Hz on postural tremor and 7.501 Hz on action tremor. On studies of short-latency somatosensory evoked potential, all patients showed a lack of the N20 component, the potential of the somatic sensory area.
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View Article and Find Full Text PDFTherapeutic potential of 4-phenylbutyric acid against methylmercury-induced neuronal cell death in mice.
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Methylmercury (MeHg) is an environmental neurotoxin that induces damage to the central nervous system and is the causative agent in Minamata disease. The mechanisms underlying MeHg neurotoxicity remain largely unknown, and there is a need for effective therapeutic agents, such as those that target MeHg-induced endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), which is activated as a defense mechanism. We investigated whether intraperitoneal administration of the chemical chaperone, 4-phenylbutyric acid (4-PBA), at 120 mg/kg/day can alleviate neurotoxicity in the brains of mice administered 50 ppm MeHg in drinking water for 5 weeks.
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