Ana Maria Cuervo
Albert Einstein College of Medicine
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Primary Section: 42, Medical Physiology and Metabolism Secondary Section: 22, Cellular and Developmental Biology Membership Type:
Member
(elected 2019)
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Biosketch
Ana Maria Cuervo is a cell biologist and physician researcher recognized for her studies on autophagy and how malfunction of this cellular process contributes to aging, neurodegenerative and metabolic disorders. Cuervo was born in Barcelona, Spain. She obtained her M.D. and Ph.D. in Biochemistry and Molecular biology from the University of Valencia in 1990 and 1994, respectively, and received postdoctoral training at Tufts University, Boston. In 2002, she started her laboratory at the Albert Einstein College of Medicine. Cuervo has been the recipient of the P. Benson Award, Keith Porter Fellow, Nathan Shock Memorial Award, Vincent Cristofalo Award, Bennett J. Cohen Award, Marshall Horwitz Prize and the Saul Korey Prize in Translational Medicine. She has delivered prominent lectures such as the NIH Director's, the Roy Walford, the Feodor Lynen, the Margaret Pittman, the David H. Murdoxk, the Gerry Aurbach, the SEBBM L'Oreal-UNESCO for Women in Science, the C. Ronald Kahn and the Harvey Lecture. Cuervo is included in the Highly Cited Researchers List (top 1% cited researchers). She is elected member of the Royal Academy of Medicine of the Valencia Community, Royal Academy of Science of Spain, the American Academy of Arts and Sciences and the National Academy of Sciences.
Research Interests
Ana Maria Cuervo's group is interested in understanding how proteins and organelles are normally turned over by the lysosomal system (autophagy) and how malfunction of autophagy in aging is linked to age-related disorders including neurodegenerative and metabolic diseases. Her studies challenged the generally accepted idea that degradation in lysosomes was not selective and lead to the discovery of selective forms of autophagy including chaperone-mediated autophagy, endosomal microautophagy and lipophagy. Using biochemical and cell biology approaches they are performing the molecular dissection of these different autophagic pathways. To understand the physiological relevance of selective autophagy, they have used genetic mouse models and demonstrated the contribution of this process to regulation of cellular metabolism, quality control and selective remodeling of the proteome. They have also demonstrated disease-specific defects on the basis for autophagic failure in different neurodegenerative disorders. Cuervo identified that chaperone-mediated autophagy decreases with age and using regulatable transgenic mouse models they demonstrated that restoration of normal autophagy function in old organisms preserves organ function. Cuervo's work has contributed to the idea of proteostasis failure in the basis for aging and age-related diseases and that autophagy is a modulable process that can be targeted with therapeutic purposes and to extend health-span.
