Bio: Dr. Aschner will focus on several topics related to pertinent public health issues in China, namely exposures to mercury and manganese. He will address to role of: (1) modulation of C. elegans genes (aat, skn-1, daf-16) that are homologous to mammalian regulators of methylmercury (MeHg) uptake and cellular resistance will modify dopaminergic neurodegeneration in response to mercury exposure,  (2) Nrf2 (a master regulator of antioxidant responses) in coordinating the upregulation of cytoprotective genes that combat mercury-induced oxidative injury, and genetic and biochemical changes that negatively impact upon Nrf2 function, (3) PARK2, a strong PD genetic risk factor, in altering neuronal vulnerability to modifiers of cellular manganese status, particularly at the level of mitochondrial dysfunction and oxidative stress. He will emphasize key findings from his 40-year scientific career that (1) shed novel mechanistic insight into metal-induced neurodegeneration; (2) identify targets for genetic or pharmacologic modulation of neurodegenerative disorders; (3) increase knowledge of the pathway involved in oxidative stress; (4) develop improved research models for human disease using knowledge of environmental sciences.

Abstract: Over the past four decades, research led by Dr. Michael Aschner has fundamentally advanced our understanding of heavy metal neurotoxicity across biological systems—from simple invertebrate models to complex mammalian brains. This body of work has elucidated the molecular, cellular, and systemic effects of metals such as methylmercury, lead, manganese, and arsenic, leveraging a multidisciplinary toolkit spanning C. elegans, rodents, and human studies. Pioneering use of C. elegans enabled high-throughput insights into metal-induced oxidative stress, mitochondrial dysfunction, and dopaminergic neurodegeneration, offering mechanistic parallels to human neuropathologies such as Parkinson’s disease. In parallel, translational investigations have characterized critical windows of susceptibility, neurodevelopmental impacts, and gene-environment interactions in mammalian and human populations. Through integration of molecular neurobiology, toxicogenomics, and epidemiology, this research continuum has informed risk assessment, therapeutic targeting, and public health policy. Dr. Aschner’s work exemplifies the power of model organisms in uncovering conserved neurotoxic pathways, laying the foundation for precision neurotoxicology in the era of environmental health.