My Research Interests:
My primary research interest is the role of mitochondria in health and aging. This former endosymbiont empowered the emergence of complex life but may also be our downfall. Mitochondrial dysfunction contributes to neurodegenerative diseases, cancer and other devastating pathologies, including aging itself. I am interested in using comparative biology to find ways that relatively long-lived species are able to maintain mitochondrial function. I believe that adaptations evolved by birds and bats to meet the metabolic demands of flight may also contribute to their relative longevity.
Why I Pursued Aging Research:
The past century has seen great progress in overcoming many diseases that were once major causes of human mortality and reduced quality of life. We are at a point were age-associated decline is now the single greatest risk factor for most major diseases, which include cardiovascular disease, sarcopenia, cancer, and dementia. Aging itself erodes quality of life, makes us increasingly susceptible to other pathology and is the ultimate cause of death if we do not succumb to another first. The desire to ameliorate the effects of age and even extend human health and lifespan was one of my primary motivations to pursue research and still is the goal for which I strive.
My Future Plans:
My ultimate goal is to continue studying the role of mitochondria in aging as an independent investigator at a research-focused university. I believe that using a multi-system approach, combining insights gained from cross-species comparative biology and the tractability of model organisms such as Drosophila melanogaster and Caenorhabditis elegans, will be a powerful way to find novel targets and therapies that can benefit humans.
Awards and Honors:
- 2013 NIA T32 Biology of Aging Training Grant
- 2012 Glenn Foundation Doctoral Student Fellowship in the Biology of Aging
- 2011 Liberal Arts & Sciences Undergraduate Research Initiative
Munkácsy E*, Khan MH*, Lane RK, Borror MB, Park JH, Bokov AF, Fisher AL, Link CD, Rea SL. DLK-1, SEK-3 and PMK-3 Are Required for the Life Extension Induced by Mitochondrial Bioenergetic Disruption in C. elegans. PLoS Genetics 2016 Jul 15;12(7):e1006133.
Munkácsy E*, Mishur RJ*, Khan M*, , Sharma L, Bokov A, Beam H, Radetskaya O, Borror M, Lane R, Bai Y, Rea SL. Mitochondrial metabolites extend lifespan. Aging Cell. 2016 Apr;15(2):336-48. doi: 10.1111/acel.12439.
Larson J, Munkácsy E, Theta-Burst LTP. Brain Research 2015 Sep 24;1621:38-50.
Munkácsy E, Rea SL. The Paradox of Mitochondrial Dysfunction and Extended Longevity. Experimental Gerontololgy 2014 Aug;56:221-233.
Khan MH*, Ligon M*, Hussey LR*, Hufnal B, Farber R 2nd, Munkácsy E, Rodriguez A, Dillow A, Kahlig E, Rea SL. TAF-4 is required for the life extension of isp-1, clk-1, and tpk-1 Mit mutants. Aging 2013 Oct;5(10):741-758.
*authors contributed equally