Brand Lab

Martin Brand, PhD


Exploring altered energy metabolism and free radical production in aging and disease.

Lab focus

The Brand lab is focused on the role of mitochondria in health, disease, and aging. Mitochondria are subcellular structures in which nutrients are oxidized to extract their energy content in the process of oxidative phosphorylation. This energy is then distributed to the rest of the cell to drive the essential machinery of life. However, in addition to releasing energy, nutrient oxidation also produces free radicals and other reactive oxygen species. Impaired energy distribution and excessive free-radical production are thought to be among the primary drivers of aging and age-related disease.


The Brand lab has pioneered new approaches to better understand mitochondrial function and dysfunction within cells and has applied these approaches to investigate the role of mitochondrial energy metabolism in aging and disease. To investigate free-radical production, we have characterized the specific sites and regulation of mitochondrial superoxide and hydrogen peroxide generation and are studying how these sites contribute to cellular oxidative stress and damage. Using high-throughput screening, we have identified novel suppressors of radical formation that do not inhibit energy metabolism, and we are using these exciting new molecules to probe and modulate mitochondrial radical production in cell and animal models of aging and disease.

Why it matters

We envision treatments that would minimize the production of free radicals by mitochondria without inhibiting energy metabolism. Our lab is collaborating with others both inside and outside the Buck to evaluate and mitigate the role of dysfunctional mitochondria in aging and in diseases of aging, including diabetes, cancer, hearing and vision loss, mobility, osteoporosis, heart and kidney disease, stroke, Parkinson’s, Alzheimer’s, and Huntington’s. Research has already opened up new possibilities for the control of these conditions. We aim to cut through the guesswork and establish how free radicals that impact aging and disease are generated and how they can be decreased.

We aim to suppress excessive mitochondrial formation of free radicals to delay or prevent many age-related diseases.

Martin Brand, PhD

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

Dr. Brand was trained in the United Kingdom at the University of Manchester Institute of Science and Technology, where he received his Bachelor of Science, and at the University of Bristol, where he received his PhD. His postdoctoral work was completed at Johns Hopkins University in Baltimore, Maryland, with Professor A.L. Lehninger. Dr. Brand was a faculty member of the Biochemistry Department at the University of Cambridge and then a group leader at the Medical Research Council in Cambridge. He moved his laboratory to the Buck Institute in 2008. Dr. Brand has made major contributions to understanding the mechanisms of energy transformation and the mechanisms of energetic inefficiency and free-radical production and their roles in evolution, physiology, and the diseases of aging.

Dr. Brand has published over 340 scientific papers, which have been cited more than 33,000 times by other scientists. His research has been recognized with the Keilin Medal of the Biochemical Society and a senior scholarship from the Ellison Medical Foundation, and with his election as a fellow of the Academy of Medical Sciences. He serves on the editorial boards of several scientific journals and the scientific advisory boards of various biotech companies.

  • Mark Watson, PhD  Postdoctoral Research Scholar

    Dr. Watson received his bachelor’s degree in biomedical science and his PhD in infection and immunity from the University of Birmingham in the United Kingdom. His research focuses on the implications of mitochondrial ROS in initiating and exacerbating diseases as well as the involvement of intestinal health in aging. Mark serves as a Buck Ambassador, providing scientific outreach to the community.

Cindy Curtice
Administrative Lab Coordinator
Phone: 415-209-2030
Selected Publications
  • Wong, H. S., Mezera, V., Dighe, P., Melov, S., Gerencser, A. A., Sweis, R. F., Pliushchev, M., Wang, Z., Esbenshade, T., McKibben, B., Riedmaier, S., Brand, M. D. (2021). Superoxide produced by mitochondrial site IQ inactivates cardiac succinate dehydrogenase and induces hepatic steatosis in Sod2 knockout mice. Free Radical Biology and Medicine, 164, 223-232. doi: 10.1016/j.freeradbiomed.2020.12.447
  • Brand, M. D. (2020). Riding the tiger – physiological and pathological effects of superoxide and hydrogen peroxide generated in the mitochondrial matrix. Critical Reviews in Biochemistry and Molecular Biology, 55, 592-661. doi: 10.1080/10409238.2020.1828258
  • Fang, J., Wong, H. S., Brand, M. D. (2020). Production of superoxide and hydrogen peroxide in the mitochondrial matrix is dominated by site IQ of complex I in diverse cell lines. Redox Biology, 37, 101722. Online 20200921. doi: 10.1016/j.redox.2020.101722
  • Wong, H. S., Monternier, P. A., Brand, M. D. (2019). S1QELs suppress mitochondrial superoxide/hydrogen peroxide production from site IQ without inhibiting reverse electron flow through Complex I. Free Radical Biology and Medicine, 143, 545-559. doi: 10.1016/j.freeradbiomed.2019.09.006
  • Mookerjee, S. A., Gerencser, A. A., Nicholls, D. G., Brand, M. D. (2017). Quantifying rates, pathways and flexibility of intracellular ATP production and consumption using extracellular flux measurements. Journal of Biological Chemistry, 292, 7189–7207. DOI: 10.1074/jbc.M116.774471. Corrections: DOI 10.1074/jbc.AAC118.004855.
  • Brand, M. D., Goncalves, R. L. S., Orr, A. L., Vargas, L., Gerencser, A. A., Borch Jensen, M., Wang, Y. T., Melov, S., Turk, C. N., Matzen, J. T., Dardov, V. J., Petrassi, H. M., Meeusen, S. L., Perevoshchikova, I. V., Jasper, H., Brookes, P. S., Ainscow, E. K. (2016). Suppressors of superoxide/H2O2 production at site IQ of mitochondrial complex I protect against stem cell hyperplasia and ischemia/reperfusion injury. Cell Metabolism, 24, 582–592. DOI: 10.1016/j.cmet.2016.08.012.

Dr. Brand’s NCBI Bibliography link

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