My Research Interests:
I am interested in the cellular mechanisms underlying the pathogenesis of tauopathies, a group of age-related neurodegenerative disorders, including Alzheimer’s disease, that are characterized by the aberrant aggregation of pathological tau proteins in the brain. I am currently investigating the down-stream consequences of tau-induced dysfunction of the nuclear lamina, a filamentous protein network that lines the interior of the inner nuclear membrane. We have found that tau-induced over-stabilization of filamentous actin, which interacts with the nuclear lamina through the linker of nucleoskeleton and cytoskeleton (LINC) complex, causes nuclear envelope invagination, heterochromatin relaxation and subsequent cell death. Interestingly, increased nuclear invagination has also been reported to occur in normal physiological aging, suggesting that exacerbation of this process by tau may underlie the association between aging and an increased risk of developing Alzheimer’s disease and related tauopathies.
Why I Pursued Aging Research:
Aging is the single most important risk factor for the development of neurodegenerative dementias. As life-expectancy increases, the prevalence of these currently incurable diseases will no doubt follow suite. Having witnessed the incredibly devastating effects of dementia firsthand, both on those afflicted and their caregivers, I strive to be able to contribute to the growing body of knowledge in this field.
My Future Plans:
I wish to pursue a tenure track faculty position at a major research university.
Awards and Honors:
- 2017 NIA T32 Biology of Aging Training Grant, UT Health San Antonio
- 2016 Outstanding Teaching Award, University of Texas at Austin
- 2014 F.M. Jones and H.L. Bruce Endowed Graduate Fellowship in Addiction Bioloy, University of Texas at Austin
- 2013 Frayne Graduate Fellowship in Addiction Biology, University of Texas at Austin
- 2006 Provost's Scholarship, Arizona State University
Cornelison, GL, Daszkowski, A, Pflanz, NC, Mihic, SJ. 2017. Interactions between zinc and allosteric modulators of the glycine receptor. J. Pharmacol. Exp. Ther. 361: 1-8.
Cornelison, GL, Pflanz, NC, Tipps, ME, Mihic, SJ. 2016. Identification and characterization of heptapeptide modulators of the glycine receptor. Eur. J. Pharmacol. 780: 252-259.
Cornelison, GL, Mihic SJ. 2014. Contaminating levels of zinc found in commonly-used labware affect glycine receptor currents. Brain Res. Bull. 100:1-5.
Kirson, D, Cornelison GL, Philpo, AE, Todorovic, J, and Mihic, SJ. 2013. Physiological concentrations of zinc reduce taurine-activated GlyR responses to drugs of abuse. Neuropharmacol. 75: 286-294.
Haydel, SE, Malhotra, V, Cornelison, GL, Clark-Curtiss, JE. 2012. The prrAB two-component system is essential for Mycobacterium tuberculosis viability and is induced under nitrogen-limiting conditions. J. Bacteriol. 194: 354-361.