Methylmercury Interactions With Gut Microbiota and Potential Modulation of Neurogenic Niches in the Brain

• Autor(a) principal: Pinto, Daniel V.
• Data de Publicação: 2020
• Outros Autores: Raposo, Ramon S., Matos, Gabriella A., Alvarez-Leite, Jacqueline I., Malva, João O., Oriá, Reinaldo B.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10316/106118; https://doi.org/10.3389/fnins.2020.576543
• topic: methylmercury; neurogenesis; brain; intestinal microbiota; neurodegenerative diseases; gut dysbiosis

Mercury (Hg) is a well-recognized biohazard for the nervous system. Methylmercury (MeHg) is an organic methylated form of Hg, highly toxic to humans, targeting the brain, as MeHg is rapidly absorbed, and easily reaches and crosses the blood-brain barrier (Takahashi et al., 2017). Neurological symptoms may vary from acute motor and visual effects to marked behavioral and psychiatric alterations. At higher neurotoxic levels, MeHg can lead to irreversible coma and, ultimately, death. It has been highlighted that MeHg long-term and low-grade toxicity may be associated with neurodegenerative disorders and perhaps a direct causality for Alzheimer’s disease (Siblerud et al., 2019). Although MeHg harmful effects to the brain have been thoroughly documented in the literature, such as increased oxidative stress and mitochondrial dysfunction, halted glutamate uptake by astrocytes and overt glutamate excitotoxicity, and activation of neuronal apoptosis cascades (Antunes dos Santos et al., 2016), less is known how MeHg affects the hippocampal neurogenic niche. Hence, in this opinion paper, we summarize up-to-date literature addressing MeHg effects on the intestinal microbiota, a key player influencing MeHg bioavailability and MeHg induction of intestinal dysbiosis (and vice-versa), and related intricate mechanisms during homeostasis and disease states. In addition, we discuss possible ways how MeHg may affect hippocampal neurogenesis and the potential lasting consequences for brain neurodegeneration.