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  • Michael Aschner, Ph.D.

Michael Aschner, Ph.D.

Michael Aschner

Professor, Department of Molecular Pharmacology

Professor, Dominick P. Purpura Department of Neuroscience

Professor, Department of Pediatrics

Harold & Muriel Block Chair in Molecular Pharmacology

Director, Einstein Center of Toxicology

Area of Research: Mechanisms of manganese-induced neurotoxicity, genetic factors associated with manganese toxicity, the role of dopamine signaling in susceptibility of dopaminergic neurodegeneration, metals in restless legs syndrome.

Contact Information

718.430.2317718.430.8922

Albert Einstein College of Medicine
Jack and Pearl Resnick Campus

1300 Morris Park Avenue
Forchheimer Building, Room 209
Bronx, NY 10461

Research ProfilesPubMed Portal

More Resources: Lab WebsiteDepartment of Molecular Pharmacology

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Professional Interests

Research in our laboratory focuses on the interaction between genetics and the environment in triggering disease both during central nervous system (CNS) development and senescence. We are addressing metal uptake across the blood-brain barrier (BBB) and distribution in the brain (neurons and glia), specifically with methylmercury (MeHg) and manganese (Mn), as well as their cellular and molecular mechanisms of neurotoxicity. Our studies address mechanisms of transport and neurodegeneration in various experimental models (C. elegans, tissue cultures and rodents), as well as follow-up on the sequalae of heavy metal deposition in the brains of human neonates by means of magnetic resonance imaging (MRI).

Hypotheses presently tested include the following: (1) Modulation of C. elegans genes (aat, skn-1, daf-16) that are homologous to mammalian regulators of MeHg uptake and cellular resistance will modify dopaminergic neurodegeneration in response to MeHg exposure. (2) Under conditions of MeHg-induced oxidative stress, Nrf2 (a master regulator of antioxidant responses) coordinates the upregulation of cytoprotective genes that combat MeHg-induced oxidative injury, and that genetic and biochemical changes that negatively impact upon Nrf2 function increase MeHg’s neurotoxicity. (3) PARK2, a strong PD genetic risk factor, alters neuronal vulnerability to modifiers of cellular Mn status, particularly at the level of mitochondrial dysfunction and oxidative stress.

Our studies are ultimately designed to (1) shed novel mechanistic insight into metal-induced neurodegeneration; (2) provide novel targets for genetic or pharmacologic modulation of neurodegenerative disorders; (3) increase knowledge of the pathway involved in oxidative stress, a common etiologic factor in neurodegenerative disorders; (4) develop improved research models for human disease using knowledge of environmental sciences.


Selected Publications

Results: (most recent)

Yang B, Bai Y, Yin C, Qian H, Xing G,Wang S, Li F, Bian J, Aschner M, Lu R. Activation of autophagic flux and the Nrf2/ARE signaling pathway by hydrogen sulfide protects against acrylonitrile-induced neurotoxicity in primary rat astrocytes. Arch Toxicol 2018; 92:2093-2108.

Rohn I, Marschall TA, Kroepfl N, Jensen KB, Aschner M, Tuck S, Kuehnelt K, Schwerdtle T, Bornhorst J. Selenium species-dependent toxicity, bioavailability and metabolic transformations in Caenorhabditis elegans. Metallomics 2018; 10:818-827.

da Cruz I, Machado M, Ribeiro E, Aschner M, Arantes L, Zamberlan D, Soares FA.Mechanisms involved in anti-aging effects of guarana (Paullinia cupana) in Caenorhabditis elegans. Brazilian J Med Biol Res2018;51:e7552.

Pinkas A, da Cunha Martins A, Jr, Aschner M. C. elegans– an emerging model for metal-induced RAGE-related pathologies. Internat J Environ Res Public Health, 15(7). pii: E1407. doi: 10.3390/ijerph15071407.

Aschner M, Autrup H, Berry CL, Boobis AR, Cohen SM, Dekant W, Galli CL, Goodman JI, Gori GB, Greim HA, Kaminski NE, Klaassen CD, Klaunig JE, Lotti M, Marquardt HW, Moretto A, Pelkonen O, Sipes IG, Wallace KB, Yamazaki H. Obfuscating transparency. Regulatory Toxicol Pharmacol 2018: 97; A1-A3.

Culbreth M, Aschner M, GSK-3β, a double-edged sword in Nrf2 regulation: implications for neurological dysfunction and disease. F1000Res 2018; 7:1043. doi: 10.12688/f1000research.15239.1.

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