Abstract

Worldwide environmental tragedies of anthropogenic origin causing massive release of metals and other pollutants have been increasing considerably. These pollution outbreaks affect the ecosystems and impact human health. Among those tragedies, recent large-scale environmental disasters in Brazil strongly affected riverside populations, leading to high-risk exposure to methylmercury (MeHg). MeHg is highly neurotoxic to the developing brain. This toxicant causes neural stem cell dysfunction and neurodevelopmental abnormalities. However, less is known about the effects of MeHg in the postnatal neurogenic niche, which harbors neural stem cells and their progeny, in the adult brain. Therefore, taking in consideration the impact of MeHg in human health it is urgent to clarify possible associations between exposure to mercury, accelerated cognitive decline, and neurodegenerative diseases. In this perspectives paper, we discuss the neurotoxic mechanisms of MeHg on postnatal neurogenesis and the putative implications associated with accelerated brain aging and early-onset cognitive decline in populations highly exposed to this environmental neurotoxicant.

Highlights

  • Methylmercury (MeHg) is considered extremely neurotoxic to the developing brain and chronic exposure to this environmental neurotoxicant may be associated with increased risk of accelerated cognitive decline and neurodegenerative diseases

  • Populations exposed to MeHg, including those affected by environmental disasters in Brazil, may be more vulnerable to severe neurological outcomes

  • In addition to the wellrecognized neurodevelopmental toxic effect of mercury, it is important to highlight the possible mild cognitive impairments derived from mercury-induced accelerated brain aging

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Summary

INTRODUCTION

Methylmercury (MeHg) is considered extremely neurotoxic to the developing brain and chronic exposure to this environmental neurotoxicant may be associated with increased risk of accelerated cognitive decline and neurodegenerative diseases. It is relevant to understand how and if MeHg affects the quality of the neurogenic niches, where NSCs and neural progenitor cells (NPCs) persist and produce neurons and glial cells (astrocytes and oligodendrocytes) across the life course This still highly unexplored research avenue may reveal a strong influence of MeHg in adult neurogenesis, impacting the quality of cognitive resources with putative important consequences for cognitive performance and memory (Sokolowski et al, 2013; Tian et al, 2016). Nowadays, it is well-established that in the adult mammalian brain new neurons are generated continuously in restricted niches and that these newborn cells are functionally integrated into existing neuronal circuits (Gage, 2000). These cells have high proliferative activity and can generate 2a and 2b phenotypes in their differentiation program, leading to newborn granular neurons and their functional integration into existing hippocampal neuronal circuits (Kempermann et al, 2018)

DISCUSSION
Conclusions and Future Perspective
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