Corinne Lasmezas
Academic Editor

Corinne I. Lasmezas


Corinne Lasmézas, DVM, Ph.D. serves as a Professor at The Scripps Research Institute. Since Dr. Lasmézas' appointment at Scripps in 2005, she has focused on how misfolded proteins lead to neuronal dysfunction and loss in diseases including Alzheimer’s, Parkinson’s and prion diseases. Additionally, Dr. Lasmézas is a reviewer for national and private funding agencies worldwide, including the US National Institutes of Health (NIH) and the UK Medical Research Council and an Advisor for the US Food and Drug Administration (FDA), the US Environmental Protection Agency (EPA) and the US Department of Agriculture (USDA). Earlier in her career, Dr. Lasmézas’ research provided the first experimental evidence that the prion disease “mad cow disease” had been transmitted to humans, causing variant Creutzfeldt-Jakob disease. At the peak of the mad cow crisis, Dr. Lasmézas became an advisor to the World Health Organization (WHO) as well as several governmental and public health committees. She is multiple TED speaker and is an internationally recognized expert in the field of neurodegenerative diseases. She has published more than 60 original scientific papers. She has been a Member of Scientific Advisory Board at Anavex Life Sciences Corp. since March 2015. Dr. Lasmézas holds a PhD in Neurosciences from the University Pierre & Marie Curie in Paris and obtained her Doctorate of Veterinary Medicine and Diploma of Aeronautic and Space Medicine from the University of Toulouse, France.

Cell Biology Infectious Diseases Neurology Neuroscience

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Professor of Neuroscience, Immunology and Microbial Science

The Scripps Research Institute
Neuroscience, Immunology and Microbial Science/Neuroscience
Our laboratory focuses on the study of neurodegenerative diseases, especially those linked to protein misfolding (protein misfolding neurodegenerative diseases, or PMNDs). These diseases comprise Alzheimer's, Parkinson's, Huntington's, prion diseases, fronto-temporal dementia, and amyotrophic lateral sclerosis. None of them are curable. They are all due to host proteins loosing their natural, functional conformation and adopting a new shape that renders them neurotoxic and prone to aggregation. Our aim is the development of novel, disease-modifying therapeutic approaches for protein misfolding neurodegenerative diseases. We think that this aim will be best achieved by intervention strategies based on blocking prion-like propagation on one hand, and the neurodegenerative process on the other hand. We are pursuing both goals by studying the underlying biology, defining therapeutic targets, identifying active molecules by high-throughput screening and developing lead compounds. The latter two tasks are performed in collaboration with our lead identification and chemist colleagues at Scripps Florida.

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