Kapahi Lab

Pankaj Kapahi, PhD

Professor

Understanding the role of nutrient signaling and metabolism in aging and age-related diseases.

Lab focus

Dietary restriction (DR), the reduction in nutrient intake without malnutrition, has been well documented as a means to extend lifespan and slow age-related diseases in many systems. We and others have previously demonstrated that lifespan extension by inhibition of the TOR pathway overlaps with the effects of DR in D. melanogaster, S. cerevisiae, and C. elegans. However, other DR response mechanisms exist that remain undiscovered. The overall goal of the Kapahi lab is to understand how an organism responds to nutrient status to influence health and disease.

We utilize worms, flies, and mice as model systems to understand how nutrients influence age-related changes in specific tissues and disease processes. We take creative approaches to develop models for various human diseases that are influenced by nutrient status using invertebrates. We study how various physiological and molecular processes, including fat metabolism, circadian clocks, advanced glycation end products, calcification, and intestinal permeability, are influenced by nutrients to impact organismal health and survival. We collaborate with multiple groups at University of California, San Francisco, and University of California, Berkeley, to undertake interdisciplinary approaches to translate our findings from multiple models to humans.

Some of the questions the Kapahi lab are asking:

  1. What genes and metabolites can act as Calorie restriction mimetics and slow aging?
  2. How does excess glucose mediate its toxicity through glycation?
  3. What factors in flies and mammalian cells mediate partial reprogramming to rejuvenate tissue health?
  4. What is the role of the brain-ovary axis in modulating ovarian aging and the detrimental effects of menopause?

Why it matters

Our work has relevance to certain age-related human diseases, including diabetes, Alzheimer’s disease, kidney stone formation, intestinal diseases, and obesity. There is an ongoing debate about the limitation of lifespan as a measure of aging and the need to assess healthspan to find the most promising interventions for humans. Through functional measures of different tissue functions and disease models, we are also examining the relationship between healthspan and lifespan.

Our work on aging in simple animals has led to real possibilities of treating human diseases, something I never thought possible when I began my career.

Pankaj Kapahi, PhD

The Kapahi lab is pleased to acknowledge the generous support of the following major funders:

Dr. Kapahi received his PhD from the University of Manchester, where he worked with Tom Kirkwood. He did his postdoctoral work with Seymour Benzer at Caltech and Michael Karin at University of California, San Diego. He joined the Buck Institute as an assistant professor in 2004.

Dr. Kapahi has published more than 80 scientific papers and holds three current patents. He has been recognized for his scientific excellence with many awards, including the Eureka Award from the National Institute on Aging, a New Scholar Award from the Ellison Medical Foundation, a Glenn Award for Research in Biological Mechanisms of Aging, the Nathan Shock Young Investigator Award, and the Breakthrough in Gerontology and Julie Martin Mid-career awards from AFAR. He currently serves on the editorial board of Aging Cell, Aging, and PLOS Genetics. Dr. Kapahi also initiated the first master’s degree course in gerontology at the Buck Institute.

  • Faisal Ahmad  Dominican University of California Graduate Student Intern

    Faisal is a graduate student at Dominican University pursuing M.S. in Biological Sciences and joined the Kapahi Lab in June 2024. He graduated from University of Illinois at Urbana Champaign with a degree in Behavioral Neuroscience and Molecular Cell Biology. He previously worked at the Cellular Neuroimaging Lab with Dr. Alicia Best-Popescu to study genes associated with aging and their effect on cellular integrity and senescence. His work at Buck centers around testing gene targets for aging interventions and exploring cellular rejuvenation by testing gene expression associated with aging in Drosophila.

    FAhmad@buckinstitute.org

  • Sudipta Bar  Postdoctoral Researcher

    Dr. Bar joined the Kapahi lab as a postdoctoral research fellow in July 2018. He received his Ph.D. in Biological Sciences from Indian Institute of Science Education and Research Kolkata, India where he studied lysosomal storage disorders using Drosophila and cell culture. At Buck, he utilizes Drosophila genetics, molecular biology, and bioinformatics tools to understand the environmental and genetic factors responsible for neurodegeneration in Alzheimer’s and related diseases. He recently received the Larry L. Hillblom postdoctoral fellowship grant (2019).

    SBar@buckinstitute.org

  • Lizbeth Enriquez  Lab Manager / Research Associate

    Lizbeth is a graduate student who joined the Kapahi Lab in 2021. She attended Dominican University of California where she received her bachelor's degree in molecular biology. Her research at the Buck Institute aims to understand the function of advanced glycation end products (AGEs) in aging and age-related disorders using in vivo mammalian model systems.

    LEnriquez@buckinstitute.org

  • Lindsay Gann  Dominican University Graduate Student

    Lindsay is a master’s student at Dominican University of California. She received a bachelor’s degree in biochemistry with a minor in anthropology from Arizona State University, as well as a bachelor’s degree in English from Trinity International University. Lindsay’s research is focused on understanding the role of cellular senescence in age-related conditions such as menopause and obesity using the drosophila model organism.

    LGann@buckinstitute.org

  • Myla Gupta  Dominican University Graduate Student

    Myla is a graduate student at Dominican University pursuing an M.S. in biological sciences. She recently graduated from UCSB with a B.S. in biological sciences, where she worked as a research assistant in the Simpson Lab studying the neural mechanics of Drosophila motor coordination. This undergrad research developed her curiosity for neuroscience and led Myla to her current projects in the Kapahi Lab, where she is investigating neural expression of genes that drive aging in a Drosophila model. She hopes to contribute to research in neurodegeneration to help ease the chronic suffering that often accompanies age."

    MGupta@buckinstitute.org

  • Worthy Gutierrez  Dominican University Graduate Student

    WGutierrez@buckinstitute.org

  • Steven Jensen, PhD  Postdoctoral Researcher

    sjensen@buckinstitute.org

  • Kiyomi Kaneshiro, PhD  Postdoctoral Researcher

    Kiyomi joined the Kapahi lab as a postdoctoral research fellow under the co-mentorship of Judith Campisi in 2021. She received her PhD from UC Santa Cruz where her research focused on understanding epigenetic inheritance using the model organism C. elegans. Her research at the Buck Institute, aims to understand the role of advanced glycation end products (AGEs) in cellular senescence and age-related neurodegenerative diseases using in vitro and in vivo mammalian model systems.

    KKaneshiro@buckinstitute.org

  • Johnathan Rylee, PhD  Postdoctoral Researcher

    Johnathan joined the Kapahi lab as a postdoc in March 2024. He received his PhD from Indiana University where he studied the genetics of photoreceptor differentiation and disease using Drosophila and zebrafish. He is interested in eye aging, and how photoreceptor lipid profiles are maintained throughout their lifespan.

    JRylee@buckinsitute.org

  • Parminder Singh, PhD  Postdoctoral Researcher

    Dr. Singh Joined Dr. Kapahi's lab as a Postdoctoral Research Fellow in the summer of 2021. He received his PhD from the National Institute of Immunology, Delhi, India. His research at the Buck Institute aims to explore the role of advanced glycation end products (AGEs) in mitochondrial disorder and addiction. He is a very affable person and spends his free time exploring and cooking spicy food.

    PSingh@buckinstitute.org

  • Praveen Singh, PhD  Postdoctoral Researcher

    psingh1@buckinstitute.org

  • Vineeta Tanwar  Research Scientist / Project Manager

    Vineeta joined the Kapahi lab as a Senior Researcher in 2022. She received her PhD from All India Institute of Medical Sciences, New Delhi, India. Her postdoctoral work at Vanderbilt University School of Medicine exploited human and mouse embryonic stem cells to optimize cardiac repair and regeneration therapy. Her continued research work at The Ohio State University in the field of Environmental Cardiology allowed her to investigate external triggers of cardiac disease, with emphasis on particulate matter exposure. She also established collaboration with United States Department of Veterans Affairs to investigate the cardio-pulmonary effects of World Trade Center (WTC) dust exposure. In her recent science industry-oriented research conducted at the Center for Integration of Science and Industry, Bentley University, she focused on quantitative measure of basic science innovation in the FDA approved drugs in the past decade with a goal to obtain more informative insight into the drug innovation trend and on health values created by biopharmaceutical companies. She is passionate about science journalism and enjoys communicating science to non-scientific audience to raise scientific awareness and fight scientific misinformation.

    VTanwar@buckinstitute.org

  • Sonny Vang  Dominican University of California Graduate Student Intern

    Sonny Vang is a master’s student who joined the Kapahi lab in July 2024. He received his bachelor’s degree in biochemistry & molecular biology with a minor in bioinformatics from the University of California, Davis. During his undergraduate education, he studied wheat ureide permease function as an intern in the Beckles lab. His research at the Buck Institute combines approaches in bioinformatics, biochemistry, and genetics to investigate novel interactions of metabolites on age-related diseases.

    SVang@buckinstitute.org

  • Radhika Vedantham  Intern

    Radhika Vedantham is a senior at Redwood High school in Larkspur with an abundance of curiosity and interest in aging research . She is an intern in Kapahi lab studying the correlation between Mannose and lifespan in C. Elegans.

  • Dipti Verma, PhD  Postdoctoral Researcher

    Dipti joined the Kapahi lab as a postdoctoral researcher in July 2024. She received her PhD from the Department of Molecular and Human Genetics, Banaras Hindu University, India where she studied the functional implications of Non-muscle myosin II Zipper in the regulation of Notch signaling in Drosophila. Her research at the Buck Institute is focused on studying the molecular mechanisms behind delayed ovarian senescence and longevity upon dietary restriction.

    DVerma@buckinstitute.org

  • Kenneth Wilson, PhD  Postdoctoral Researcher

    Kenneth received his bachelor’s degree in molecular and cell biology from University of California Berkeley, his master’s degree in biological sciences from Dominican University of California and his PhD from University of Southern California. His current research focuses on understanding how natural genetic variation can influence response to diet to affect longevity and health.

    KAWilson@buckinstitute.org

  • Yifan Xiang, MD  Postdoctoral Researcher

    Yifan joined the Kapahi Lab as a Postdoctoral Researcher in 2023. She received her MD from the Zhongshan Ophthalmic Center, Sun Yat-sen University. Her research at the Buck aims to develop prediction models for aging and age-related diseases with AI.

    YXiang@buckinstitute.org

  • Zhixin (Alice) Zhang  Research Associate

    Alice received her B.S. in bioengineering from UC Berkeley in 2022 where she studied muscle aging and rejuvenation in Dr. Irina Conboy’s lab. She joined the Buck in May 2023 as a research associate in the Campisi Lab and worked on characterizing senescent corneal cells. In May 2024, Alice joined the Kapahi Lab and started pursuing a PhD from the University of Groningen under the supervision of Dr. Kapahi and Dr. Demaria. She is studying the role of glycation stress in promoting aging and age-related disease. Outside of the lab, she enjoys being outdoors and cooking.

    zzhang@buckinstitute.org

Alice Zhang
Administrative Lab Coordinator
Zzhang@buckinstitute.org
Phone: 805-710-1189

Program 1 Genetic mechanisms by which dietary restriction (DR) confers neuroprotection

Dietary restriction (DR) is one of the most robust interventions known to extend lifespan and delay the onset of age-related diseases across species. The beneficial effects of DR are mediated through a variety of genetic, metabolic, and circadian mechanisms that confer protection at both the cellular and tissue levels. This program focuses on three critical areas where DR plays a protective role: neuroprotection and tauopathies, modulation of age-related visual decline, and tissue-specific reprogramming of aging processes. Understanding these mechanisms will inform the development of novel interventions to enhance healthspan and prevent age-related diseases.

  1. Role of DR in Tauopathy and Neuroprotection

DR provides neuroprotection by modulating key metabolic and genetic pathways, in tauopathy models and brain aging. Using Drosophila as a model system, we discovered that the OXR1 gene maintains retromer complex integrity, critical for protein and lipid trafficking. We will determine how the retromer and OXR1 influence downstream genes in fat metabolism and synaptic homeostasis to mediate its protective effects.  We have also observed that DR influences glycogen metabolism in neurons protecting them by shifting metabolic flux from glycolysis to the pentose phosphate pathway (PPP), reducing oxidative damage. These findings are being translated to mammalian models to explore how DR can mitigate tau-mediated neurodegeneration and protect against Alzheimer’s disease. This work defines a novel and conserved role for glycogen accumulation in AD and its alleviation by DR for neuroprotection.

  1. Role of DR in Eye Aging

Aging significantly impacts visual health, contributing to diseases like macular degeneration. We have found that DR enhances circadian clock function, particularly through the CLOCK transcription factor, which regulates genes involved in photoreceptor homeostasis. Our research has shown that the CLLOCK transcription factor prevents photoreceptor degeneration in flies and mice. We will further investigate the molecular mechanisms by which CLOCK protects the visual system, identifying potential genetic targets for therapeutic interventions in age-related eye diseases. We have also identified a non-invasive biomarker for aging based on retinal fundus imaging. This model’s effectiveness is further supported by genome-wide association studies (GWAS), which identify genetic loci associated with ‘eyeAge’ which are being interrogated in the fly eye.

  1. Role of DR in Tissue Reprogramming

Tissue-specific responses to DR are a key focus of our research, as DR impacts aging differently across various tissues. Our studies in Drosophila have identified specific gene expression changes in neurons in response to DR, which influence epigenetic reprogramming and developmental pathways. This work has identified genes that can partially reprogram neurons and photoreceptors These insights will inform tissue-specific therapies to combat age-related diseases.

Through its effects on neuroprotection, visual system health, and partial reprogramming, dietary restriction offers a powerful intervention to slow aging and promote longevity. This research program will advance our understanding of DR’s multifaceted role in aging and inform strategies for therapeutic interventions targeting age-related diseases.

 

Program 2 Role of Glycation in Aging and Age-Related Diseases

Glycation, a non-enzymatic process where sugars bind to proteins, leads to the formation of advanced glycation end-products (AGEs), which accumulate with age and contribute to the development of age-related diseases such as diabetes, neurodegeneration, and cardiovascular diseases. This research program focuses on the role of glycation in tissue-specific aging, its contribution to cellular senescence, and its impact on insulin resistance (IR). Our long-term goal is to explore the therapeutic potential of glycation-lowering interventions to mitigate these aging processes.

  1. Role of Glycation in Tissue-Specific Aging

Glycation accelerates tissue-specific aging by driving damage in key organs, including the heart, eyes, pancreas, and muscles. Our studies in C. elegans and mice have shown that methylglyoxal (MGO)-derived AGEs promote neuronal damage and diabetic neuropathy-like symptoms. To combat this, we developed a combination therapy (Gly-Low), which includes compounds like nicotinamide, lipoic acid, and pyridoxamine. This therapy has successfully reduced MGO and AGEs in vivo, improving insulin sensitivity and extending lifespan in mice. Future studies will focus on understanding how glycation impacts different tissues at the protein level. By utilizing click-chemistry-based techniques, we will identify glycated proteins and their role in driving tissue-specific damage. This approach will provide a deeper understanding of how glycation contributes to age-related diseases across various organs.

  1. Role of Glycation in Cellular Senescence

Cellular senescence, a hallmark of aging, is closely tied to glycation. MGO, a reactive precursor to AGEs, has been shown to induce senescence in various tissues, particularly in adipose tissue and pancreatic β-cells, leading to functional decline. Our research indicates that IR exacerbates β-cell senescence, which in turn accelerates metabolic dysfunction, worsening the overall aging phenotype. To further investigate, we will study how MGO-induced glycation drives senescence in preadipocytes and β-cells. We hypothesize that glycation creates a feedback loop between insulin resistance and senescence, particularly in metabolically active tissues. Additionally, we will explore the therapeutic potential of senolytics in conjunction with Gly-Low to target and eliminate senescent cells, potentially mitigating glycation-induced IR and extending healthspan.

  1. Role of Glycation in Insulin Resistance and Diabetes

Insulin resistance is a common feature of aging and a precursor to type 2 diabetes. AGEs, especially MGO, contribute to IR by disrupting insulin signaling in adipose tissue and impairing insulin release from pancreatic β-cells. Our research has shown that glycation-induced insulin resistance is not only a driver of metabolic dysfunction but also a key factor in cellular senescence. We propose to study the interplay between MGO-induced glycation, IR, and senescence, focusing on how these processes interact within adipose tissue and the pancreas. This research will provide insight into whether glycation acts as a central mediator in these tissues and whether multiple interventions, such as Gly-Low combined with senolytics, can provide additive protection against age-related metabolic diseases.

This research program on glycation aims to uncover how tissue-specific glycation, cellular senescence, and insulin resistance contribute to aging and age-related diseases. By investigating the molecular mechanisms underlying these processes and developing glycation-lowering therapies, we hope to offer new interventions to extend healthspan and mitigate the detrimental effects of aging.

 

Program 3 Evolutionary Approaches to Study the role of reproductive traits in driving aging in women

The evolutionary theory of aging, particularly the Antagonistic Pleiotropy (AP) hypothesis, posits that genes promoting early reproductive success may increase susceptibility to age-related diseases later in life. This trade-off between fertility and longevity explains why aging accelerates post-reproduction. While much research focuses on late-life aging, early-life reproductive events such as menarche and childbirth also play critical roles in shaping aging trajectories. Our program aims to explore these evolutionary trade-offs, leveraging Mendelian randomization (MR) analyses and fly and mice models to elucidate how reproductive timing, metabolism, and diet influence aging and age-related diseases in women.

  1. Interplay Between Metabolism and Reproductive Events

Metabolites play a critical role in aging and are influenced by reproductive events. We are identifying metabolites linked to the timing of menarche and childbirth, suggesting a metabolic signature that accelerates aging. Using Drosophila melanogaster as a model, we will validate these metabolites and investigate their role in mediating aging-related outcomes. This will help establish causal links between metabolism, reproductive timing, and aging. We will also develop a predictive aging model that integrates reproductive history, metabolism, and diet for insights into personalized interventions aimed at promoting healthy aging in women.

  1. The impact of mating on aging and age-related traits in mice

The postpartum period represents a critical but understudied window of vulnerability, during which reproductive events and external stressors may exacerbate age-related decline. Animal models, particularly in mice, suggest that pregnancy can induce lasting changes in injury repair pathways, increasing the risk of metabolic dysfunction and other adverse outcomes. However, there is little research on how the postpartum environment influences maternal aging. We are exploring the impact of diet, specifically high-fat diet (HFD) and caloric restriction (CR), on age-related outcomes in C57BL/6 mice during the postpartum period. We hypothesize that elevated BMI induced by HFD accelerates aging more significantly in mated mice compared to non-mated mice, with CR providing a protective effect. We plan to study the molecular mechanisms by which elevated BMI mediates maternal programming during the postpartum period using RNA sequencing and metabolomics.

This research program aims to bridge evolutionary theory with modern biomedical research to better understand how reproductive timing, metabolism, and diet influence aging. By studying the interplay between these factors, we will identify novel genetic and metabolic targets for interventions to slow aging, improve maternal health, and reduce the risk of age-related diseases in women. These findings will contribute to predictive models that inform individualized strategies for promoting healthy aging.

 

Selected Publications
  • Wilson KA, Bar S, Dammer EB, Carrera EM, Hodge BA, Hilsabeck TAU, Bons J, Brownridge GW 3rd, Beck JN, Rose J, Granath-Panelo M, Nelson CS, Qi G, Gerencser AA, Lan J, Afenjar A, Chawla G, Brem  RB, Campeau PM, Bellen HJ, Schilling B, Seyfried NT, Ellerby LM, Kapahi P. OXR1 maintains the retromer to delay brain aging under dietary restriction. Nat Commun. 2024 Jan 11;15(1):467. doi: 10.1038/s41467-023-44343-3. PubMed PMID: 38212606; PubMed Central PMCID: PMC10784588.
  • Sara Ahadi, Kenneth A Wilson Jr, Boris Babenko, Cory Y McLean, Drew Bryant, Orion Pritchard, Ajay Kumar, Enrique M Carrera, Ricardo Lamy, Jay M Stewart, Avinash Varadarajan, Marc Berndl, Pankaj Kapahi, Ali Bashir. Longitudinal fundus imaging and its genome-wide association analysis provide evidence for a human retinal aging clock. Elife. 2023 Mar 28;12:e82364. doi: 10.7554/eLife.82364. PMCID:PMC10110236 DOI: 7554/eLife.82364
  • Hodge BA, Meyerhof GT, Katewa SD, Lian T, Lau C, Bar S, Leung NY, Li M, Li-Kroeger D, Melov S, Schilling B, Montell C, Kapahi P. Dietary restriction and the transcription factor clock delay eye aging to extend lifespan in Drosophila Melanogaster. Nat Commun. 2022 June;13(1):3156. doi: 10.1038/s41467-022-30975-4. PMCID: PMC9174495
  • Wilson KA, Chamoli M, Hilsabeck TA, Pandey M, Bansal S, Chawla G, Kapahi P. Evaluating the beneficial effects of dietary restrictions: A framework for precision nutrigeroscience. Cell Metab. 2021;33(11):2142-73.  PMCID:PMC8845500
  • Wilson KA, Beck JN, Nelson CS, Hilsabeck TA, Promislow D, Brem RB, Kapahi P GWAS for Lifespan and Decline in Climbing Ability in Flies upon Dietary Restriction Reveal decima as a Mediator of Insulin-like Peptide Production. Curr Biol. 2020 Jul 20;30(14):2749-2760
  • Jyotiska Chaudhuri, Yasmin Bains, Sanjib Guha, Arnold Kahn,David Hall, Neelanjan Bose, Alejandro Gugliucci, Pankaj Kapahi, The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality, Cell Metabolism, Volume 28, Issue 3, 4 September 2018, Pages 337-352
  • Zee, T., Bose, N., Stoller, M., Kapahi, P. Alpha-lipoic acid ameliorates stone formation in a mouse model of cystinuria. (Accepted at Nature Medicine).
  • Luis, N. M., Wang, L., Ortega, M., Deng, H., Katewa, S. D., Li, P. W., Karpac, J., Jasper, H., Kapahi, P. Intestinal IRE1 is required for increased triglyceride metabolism and longer lifespan under dietary restriction. Cell Rep, 25, 17(5), 1207–1216.
  • Chaudhuri, J., Bose, N., Gong, J., Hall, D., Rifkind, A., Bhaumik, D., Peiris, T. H., Chamoli, M., Le, C. H., Liu, J., Lithgow, G. J., Ramanathan, A., Xu, X. Z., Kapahi, P. (2016 Nov 21). A Caenorhabditis elegans model elucidates a conserved role for TRPA1-Nrf signaling in reactive α-Dicarbonyl detoxification. Curr Biol, 26(22), 3014–25.
  • Katewa, S. D., Akagi, K., Bose, N., Rakshit, K., Camarella, T., Zheng, X., Hall, D., Davis, S., Nelson, C. S., Brem, R. B., Ramanathan, A., Sehgal, A., Giebultowicz, J. M., Kapahi, P. (2016 Jan 12). Peripheral clocks modulate lifespan and fat metabolism upon dietary restriction. Cell Metab, 23(1), 143-54. doi: 10.1016/j.cmet.2015.10.014. Epub 2015 Nov 25.
  • Chen, D., Li, P. W., Goldstein, B. A., Cai, W., Thomas, E. L., Chen, F., Hubbard, A. E., Melov, S., Kapahi, P. (2013). Germline signaling mediates the synergistically prolonged longevity produced by double mutations in daf-2 and rsks-1 in C. elegans. Cell Rep, 5, 1600–10.
  • Katewa, D., Demontis, F., Kolipinski, M., Hubbard, A., Gill, M., Perrimon, N., Melov, S., Kapahi, P. (2012). Intra-myocellular triglyceride turnover plays a critical role in mediating responses to dietary restriction in Drosophila melanogaster. Cell Metab, 16, 97–103.
  • Zid, B. M., Rogers, A. N., Katewa, S. D., Vargas M. A., Kolipinski, M. C., Lu, T. A., Kapahi, P. (2009). 4E-BP extends lifespan upon dietary restriction by enhancing mitochondrial activity in Drosophila. Cell, 139, 149–60.
  • Pan, K. Z., Palter, J. E., Rogers, A. N., Olsen, A., Chen, D., Lithgow, G. J., Kapahi, P. Inhibition of mRNA translation extends lifespan in Caenorhabditis elegans. Aging Cell, 6(1), 111–9. PMID: 17266680.
  • Kapahi, P., Zid, B. M., Harper, T., Koslover, D., Sapin, V., Benzer, S. Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway. Curr Biol, 14, 885–90.
  • Rossi, A., Kapahi, P., Natoli, G., Takahashi, T., Chen, Y., Karin, M. (2000). Anti-inflammatory cyclopentenone prostaglandins are direct inhibitors of IkappaB kinase. Nature, 403(6765), 103–8.

Dr. Kapahi’s full publication list

You Are What You Eat? How Diet Boosts Brain Health

Chemical in Your Food Makes You Binge Eat, Scientists Say

Longevity willpower – understanding how AGEs affect cravings could help us age more healthily

Restrict calories to live longer, study says, but critics say more proof is needed

A calorie-restricted diet may slow aging in healthy adults, research finds

Gene Tweak Can Extend Life 500% (But You Have to Be a Worm)

ead Biologists Have Identified A Way To Extend Human Lifespan By 500%

The Role of Advanced Glycation End Products in Aging and Disease. Podcast with Pankaj Kapahi

Buck Institute study offers hope on kidney stones, gout

Exclusive Fall 2017 Membership presentation: Nutrition, Metabolism & Aging (A conversation with Professor Pankaj Kapani, PhD)

Buck research could alleviate kidney ailment

Reducing nerve-damaging reactive metabolites

New Research Provides Path to Study Diabetic Complications

Kapahi lab project on Advanced Glycation Endproducts and Diabetic Complications

Zinc May Help Drive Kidney Stone Formation

The 500-year-old man: Buck Institute research makes Jay Leno monologue

View all

Support the Buck

We rely on donations to support the science that we believe will add years to people's lifespan and decades to their healthspan.