Jon Iker Etchegaray, Ph.D.

Whether it is the brain, the eyes, the heart or the liver, organs in our body change the way they digest nutrients as they age. These changes in metabolism have been linked to the development of diseases such as Alzheimer’s, age-related vision loss, heart disease and liver failure. Another hallmark of aging is increased inflammation. Inflammation also affects most of the organs in our body, and it too has been linked with many of the same diseases.

The relationship between changes in metabolism and increased inflammation and how this relationship impacts diseases is not well understood. In the Etchegaray lab, we seek to decipher these unknowns. Our work focuses on Alzheimer’s disease and age-related vision loss, with the hope that our findings will one day lead to new treatments that can mitigate these devastating illnesses.

In mammals, the central nervous system (CNS), composed of the brain, retina, and spinal cord, is one of the most metabolically active systems in the body. Due to its high metabolic rate and low regenerative capabilities, the CNS needs to be adequately supplied with nutrients at all times. Failure to meet this metabolic demand has been shown to be associated with age-related defects, such as cognition, and is a hallmark of most, if not all, neurodegenerative and retinal diseases.

Crucial to CNS metabolism is the blood brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) in the brain and the blood-retina barrier (BRB) in the eye. Much work has been done on exploring how the BBB controls metabolism in the CNS. How the BCSFB and the BRB control metabolism in the brain and the retina respectively, remains poorly understood. The BCSFB is composed of the choroid plexus epithelium (CPE) while the BRB is made up of the retinal pigment epithelium (RPE). The CPE and RPE both constitute epithelial barriers connected by tight junctions that sit at the interface of the vasculature and the CNS. As such they regulate the transport of metabolites and hormones in and out of tissue and have similar molecular expression profiles. Furthermore, both the CPE and RPE have been heavily implicated in degenerative diseases of the CNS, including Alzheimer’s disease and age-related macular degeneration.

Therefore, investigating the role these cells play in controlling metabolism may not only further our understanding of physiology but also into our understanding of degenerative diseases in the CNS, including the development of therapeutics that target these cells to restore metabolism and potentially mitigate disease. As these cells are highly similar, in the Etchegaray lab we take advantage of the synergy they provide in studying both, and have developed a research program that studies how the epithelial barriers of the CNS control metabolism during homeostasis, inflammation, and disease

Education

B.S., Biology, Boston University, 2008
Ph.D., Neurobiology, Boston University, 2015

Honors and Awards

Travel Award, XXth International Symposium on Retinal Degeneration (RD2023) and the BrightFocus Macular Fast Track^SM, Torremolinos, Spain (Travel Award)
NIH F32 Fellowship EY031211-01, 2020
Immunology Training Grant Recipient, University of Virginia Charlottesville, 2018
Brenton R. Lutz award for Excellence in Neurobiology, Boston University, 2015

Joined OMRF scientific staff in 2024

Etchegaray, J.I., Penberthy, K., Nagasaka, Y., Paul, S., Seshadri, V., Raymond, M., Royo-Marco, A…. Ravichandran, K.S., (2023). A local source of insulin in the eye governed by phagocytosis and starvation. Nature Metabolism, 5, 207–218

Krabbe, G.*, Minami, S. S.*, Etchegaray, J. I.*, Taneja, P., Djukic, B., Davalos, D.… Gan, L., (2017). Microglial NFκB-TNFα hyperactivation induces obsessive-compulsive behavior in mouse models of progranulin-deficient frontotemporal dementia. Proceedings of the National Academy of Sciences of the United States of America, 114, 5029–5034 (*co-first authors)

Etchegaray, J.I., Tran, J., Elguero, J., Sinatra, V., Feany, M., and McCall, K., (2016). Defects in Phagocytic Corpse Processing Result in Neurodegeneration and Can Be Rescued by TORC1 Mediated Inhibition of Autophagy. Journal of Neuroscience, 36, 3170-3183 

Etchegaray, J.I.*, Timmons, A.*, Klein, A.P., Pritchett, T.L., Welch, E., Meehan, T.L., Li, C. and McCall, K., (2012) Draper acts through the JNK pathway to control synchronous engulfment of dying germline cells by follicular epithelial cells. Development, 139, 4029-4039 (*co-first authors).

Aging & Metabolism Research Program, MS 46
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, OK 73104

E-mail: iker-etchegaray@omrf.org

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Carl Van Der Linden
Research Technician III