Ana Maria Cuervo

I consider it an authentic privilege being involved in aging research at this particular time in history. When I started in medical school, aging was that irreversible condition for which the only possible course of action was to assure elders comfort. We have now reformulated aging as something that can be modified and is being modified! What can be more exciting than seeing all the knowledge generated during the past decades put at good use and with the potential of being transformative for our society?
— Ana Maria Cuervo, M.D., Ph.D

Ana Maria Cuervo, M.D., Ph.D.

Professor at albert einstein college medicine and Robert and Rene Belfer Chair for the Study of Neurodegenerative Diseases

Dr. Ana Maria Cuervo is the Robert and Renee Belfer Chair for the Study of Neurodegenerative Diseases, Professor in the Departments of Developmental and Molecular Biology and of Medicine of the Albert Einstein College of Medicine and co-director of the Einstein Institute for Aging Studies. She obtained her M.D. and Ph.D. in Biochemistry and Molecular biology from the University of Valencia (Spain) 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, where she continues her studies in the role of protein-degradation in neurodegenerative diseases and aging.

Dr. Cuervo’s group is interested in understanding how altered proteins can be eliminated from the cells through the lysosomal system (autophagy) and how malfunction of autophagy in aging is linked to age-related disorders including neurodegenerative and metabolic diseases.

Dr. Cuervo has been the recipient of prestigious awards such as the P. Benson Award, Keith Porter Fellow, Nathan Shock Memorial Lecture Award, Vincent Cristofalo Award in Aging, Bennett J. Cohen award in basic aging biology, Marshall Horwitz Prize for excellence in research and the Saul Korey Prize in Translational in Medicine Science. She has also received twice the LaDonne Schulman Teaching Award. Dr. Cuervo has delivered the Robert R. Konh Memorial Lecture, the NIH Director’s Lecture, the Roy Walford Endowed Lecture, the Feodor Lynen Lecture, the Margaret Pittman Lecture, the IUBMB Award Lecture, the David H. Murdoxk Lecture, the Gerry Aurbach Plenary Lecture, the SEBBM L’Oreal-UNESCO for Women in Science, and the Harvey Lecture. She is currently co-Editor-in-Chief of Aging Cell. Dr. Cuervo has served at the NIA Scientific Council and the NIH Council of Councils and is currently member of the NIA Board of Scientific Counselors and of the Advisory Committee to the NIH Deputy Director. In 2015 she was elected International Academic of the Royal Academy of Medicine of the Valencia Community and in 2017, she was elected member of the Real Academia de Ciencias Exactas, Fisicas y Naturales. She has recently elected member of the American Academy of Arts and Sciences.


The Cuervo lab has a long-standing expertise in the molecular mechanisms of autophagy and the contribution of malfunctioning of this process to aging and age-related disorders, including neurodegeneration, metabolic diseases and cancer. Our group identified and is currently characterizing selective forms of autophagy such as lipophagy, endosomal microautophagy and chaperone-mediated autophagy (CMA).

The goal of our studies is to understand the role that autophagic pathways, main components of the proteostasis network, have in maintenance of cellular homeostasis, quality control and cellular energetics. We are using cellular and experimental mouse models to study how autophagic processes are regulated and what are the consequences of their failure in old organisms.

Our hypothesis is that sustained challenges (metabolic excess, presence of toxic proteins, etc) can inhibit autophagic function and that conversely, a decline in autophagic function can promote chronic maladaptation in aging, thereby creating a vicious cycle that amplifies the risk for age-related disorders such as neurodegenerative diseases or metabolic derangements.

Significance: If our hypothesis is correct, interventions aimed at preventing or reverting the autophagic failure related to aging could have a great therapeutic potential against age-related diseases. In fact, our group has started the development of chemical compounds that modulate autophagic activity and that we anticipate could be used to prevent the decline of autophagy with age and thus delay prominent diseases among our elder population.

aging critical publications

  • Kaushik S, Cuervo AM. Proteostasis and aging. Nat Med. 21:1406-15, 2015.

  • Caballero B, Wang Y, Diaz A, Tasset I, Juste YR, Mandelkow E-, Mandelkow E, Cuervo AM*. Interplay of pathogenic forms of human tau with different autophagic pathways. Aging Cell 17(1): doi: 10.2222/acel.12692, 2017 PMID: 29024336

  • Bejarano E, Murray J, Wang X, Pampliega, O, Yin D, Patel B, Yuste A, Wolkoff A, Cuervo AM. Defective recruitment of motor proteins to autophagic compartments contributes to autophagic failure in aging. Aging Cell doi: 10.1111/acel.12777, 2018

  • Walter RO, Arias E, Diaz A, Burgos ES, Guan F, Tiano S, Mao K, Green CL, Oiu Y, Shah H, wang D, Hudgins AD, Tabrizian T, Tosti V, Shechter D, Fontana L, Kurland IJ, Barizilai N, Cuervo AM, Promislow DEL, Huffman DM. Sarcosine Is Uniquely Modulated by Aging and Dietary Restriction in Rodents and Humans. Cell Reports 25, P663-676, 2018

  • Kaushik K, Cuervo AM. The coming of age of Chaperone-mediated autophagy. Nat. Rev. Cell. Mol. Biol. Doi:, 2018

Additional publications

  • Cuervo, A.M.; Dice, J.F. Age-related decrease in chaperone-mediated autophagy. J. Biol. Chem  275, 31505-31513, 2000.

  • Zhang, C., Cuervo, AM*. Restoration of chaperone-mediated autophagy in aging improves cellular maintenance and organ function. Nat. Med. 14: 959-65, 2008   

  • Anguiano J, Gaerner T, Daas B, Gavathiotis E, Cuervo AM*. Chemical modulation of Chaperone-mediated autophagy by novel retinoic acid derivatives. Nat. Chem. Biol. 9:374-82, 2013

  • Schneider JL, Suh Y, Cuervo AM*.  Deficient chaperone-mediated autophagy in liver leads to metabolic disregulation. Cell Metab. 20:417-432, 2014