AREAS OF SPECIALTY:

  • Proteostasis

  • Autophagy

  • Neurodegenerative diseases

“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.

  • Distinguished Professor at The Albert Einstein College of Medicine

  • Robert and Rene Belfer Chair for the Study of Neurodegenerative Diseases

  • Board Member,  American Federation for Aging Research (AFAR)

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 the malfunction of autophagy in aging is linked to age-related disorders including neurodegenerative and metabolic diseases.

Focus Areas

  • Autophagy and its Malfunction. Dr. Cuervo aims to understand the role that autophagic pathways have in maintenance of cellular homeostasis, quality control and cellular energetics. Cuervo’s lab is using cellular and experimental mouse models to study how autophagic processes are regulated and what are the consequences of their failure in old organisms.

  • Cuervo hypothesizes that sustained functional 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.

  • If Cuervo’s hypothesis is correct, interventions aimed at preventing or reverting the autophagic failure could have a great therapeutic potential against age-related diseases.

Awards and Honors

  • 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. LaDonne Schulman Teaching Award (X2) .

  • Dr. Cuervo has delivered the NIH Director’s Lecture, the SEBBM L’Oreal-UNESCO for Women in Science Lecture and many others.

  • 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 is an elected member of the American Academy of Arts and of the National Academy of Sciences.

aging critical publications

  • Khawaja RR, Martín-Segura A, Santiago-Fernández O, Sereda R, Lindenau K, McCabe M, Macho-González A, Jafari M, Scrivo A, Gomez-Sintes R, Chavda B, Saez-Ibanez AR, Tasset I, Arias E, Xie X, Kim M, Kaushik S, Cuervo AM*. Sex- and cell type-specific loss of chaperone-mediated autophagy across tissues with aging. Nature Aging doi: 10.1038/s43587-024-00799-6. Epub ahead of print. PMID: 39910244, 2025

  • Gomez-Sintes R Xin Q, Diaz A, Garner TP, Cotto-Rios XM, Wu Y, McCabe M, Dong S, Reynolds CA, Patel B de la Villa P, Macian F, Boya P, Gavathiotis E, Cuervo AM. Targeting NCoR-RAR interaction activates chaperone-mediated autophagy and protects against retinal degeneration. Nat. Comm. 13(1): 4220, doi: 10.1038/s41467-022-31869-1, 2022

  • Bourdenx M, Martin-Segura A, Scrivo A, Rodriguez-Navarro J, Kaushik S, Tasset I, Diaz A, Strom NJ, Xin Q, Juste YR, Stevenson E, Luengo E, Clement C, Choi SJ, Krogan NJ, Mosharov EV, Santambrogio L, Grueninger F, Collin L, Swaney DL, Sulzer D, Gavathiotis E, Cuervo AM. Chaperone-mediated autophagy prevents collapse of the neuronal metastable proteome. Cell 184: 1-19 doi: 10.1016/j.cell.2021.03.048, 2021

  • Dong S, Wang Q, Kao YR, Diaz A, Tasset I, Kaushik S, Thiruthuvanathan V, Zintiridou A, Nieves E, Dzieciatkowska M, Reisz JA, Gavathiotis E, D’Alessandro A, Will B, Cuervo AM. Chaperone- mediated autophagy sustains hematopoietic stems cell function. Nature 591:117-123, 2021

  • Kaushik K, Cuervo AM. The coming of age of Chaperone-mediated autophagy. Nat. Rev. Cell. Mol. Biol. Doi: doi.org/10.1038/s41580-018-0001-6, 2018

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

Additional Publications

  • Jafari, M, Marcho-Gonzalez, A., Diaz A, Lindenau K, Santiago-Fernandez O, Zang M, Massey A C., deCabo R, Kaushik S, Cuervo AM. (2024) Calorie restriction and calorie restriction mimetics activate chaperone-mediated autophagy Proc Natl Acad Sci U S A 121(26):e2317945121. doi: 10.1073/pnas.2317945121, 2024

  • Krause GJ, Diaz A, Jafari M, Khawaja RR, Agullo-Pascual E, Santiago-Fernández O, Richards AL, Chen KH, Dmitriev P, Sun Y, See SK, Abdelmohsen K, Mazan-Mamczarz K, Krogan NJ, Gorospe M, Swaney DL, Sidoli S, Bravo-Cordero JJ, Kampmann M, Cuervo AM. Reduced endosomal microautophagy activity in aging associates with enhanced exocyst-mediated protein secretion. Aging Cell. e13713. doi: 10.1111/acel.13713, 2022

  • Juste YR, Kaushik S, Bourdenx M, Aflakpui R, Bandyopadhyay S, Garcia F, Diaz A, Lindenau K, Tu Vincent, Krause GJ, Jafari M, Singh R, Muñoz J, Macian F, Cuervo AM. Reciprocal regulation of chaperone-mediated autophagy and the circadian clock. Nat. Cell Biol. 23(12):1255-1270 10.1038/s41556-021-00800-z. 2021

  • 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 29:e12777 doi: 10.1111/acel.12777, 2018

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