Fetal minamata disease: A human episode of congenital methylmercury poisoning

Alessandra A. Dos Santos, Louis W. Chang, Grace Liejun Guo, Michael Aschner

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Scopus citations

Abstract

This chapter addresses well-known episodes of methylmercury (MeHg) poisoning, highlighting differences between the epidemics in Minamata Bay, Japan, and Iraq. Special attention is directed to the cognitive effects of MeHg in neonates and children, and the underlying changes in cytoarchitecture. Finally, we discuss the biomolecular basis of neurotoxicity in fetal Minamata disease emphasizing neural cell adhesion molecule and changes in neuronal cytoskeletal proteins. Cell polarization and migration patterns require dynamic rearrangement of the actin and microtubule cytoskeletons via intracellular signaling pathways involving Rho family GTPases. The Rho-associated protein kinases are central regulators of the actin cytoskeleton downstream of the small GTPase Rho and their role is discussed within the context of MeHg-induced injury.

Original languageEnglish (US)
Title of host publicationHandbook of Developmental Neurotoxicology
PublisherElsevier
Pages399-406
Number of pages8
ISBN (Electronic)9780128094051
DOIs
StatePublished - Jan 1 2018

Keywords

  • Methylmercury
  • Microtubules
  • Minamata disease
  • Neurotoxicity
  • Rho-associated protein kinases (ROCKs)

ASJC Scopus subject areas

  • Neuroscience(all)

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    Dos Santos, A. A., Chang, L. W., Guo, G. L., & Aschner, M. (2018). Fetal minamata disease: A human episode of congenital methylmercury poisoning. In Handbook of Developmental Neurotoxicology (pp. 399-406). Elsevier. https://doi.org/10.1016/B978-0-12-809405-1.00035-3