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Mentor: Jonathan Doorn, PhD
Year Entered Into Program: 2007-2012
PhD Institution: Department of Environmental Health, University of Cincinnati, Cincinnati, OH
The precise role of glia (e.g. microglia) in Parkinson’s disease-related neuronal death is currently unknown but is hypothesized to be significant based on previous studies. The Doorn lab is interested in determining the role of the endogenous neurotoxin, 3,4-dihydroxyphenylacetaldehyde (DOPAL), in Parkinson’s disease. Glial cells have been shown to metabolize dopamine, but the amount of DOPAL they produce via MAO oxidative deamination of dopamine is unknown, along with further metabolism of DOPAL via ALDH. My research involves investigation into the toxicity and metabolism of these dopamine metabolites via glia and activation of these cells (i.e. microglia) by such toxic intermediates.
Rees, J.N., Florang, V.R., Eckert, L.L., and Doorn, J.A.: Protein reactivity of 3,4-dihydroxyphenylacetaldehyde, a toxic dopamine metabolite, is dependent on both the aldehyde and the catechol. Chem Res Toxicol, 22, 1256-1263, 2009. PMCID: PMC2717024 [Available on 2010/7/1]
Henze, M., Hart, D., Samarel, A., Barakat, J., Eckert, L., and Scrogin, K.: Persistent alterations in heart rate variability, baroreflex sensitivity, and anxiety-like behaviors during development of heart failure in the rat. Am. J. Physiol. Heart Circ. Physiol. 295:H29-H38, 2008. PMID: 18456727
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