Mark A. Lovell

Associate Professor of Chemistry
Analytical and Biological Chemistry

319 Chemistry-Physics Building (Office)
135 Sanders-Brown Building (Laboratory)
Phone: (859) 257-7070 (Chemistry-Physics Office)
Phone: (859) 257-1412, x 251 (Sanders-Brown Office)
Phone: (859) 257-1412, x 250 or 252 (Laboratory)
FAX: (859) 323-1069
Email: malove2@uky.edu

1987, B.A., Berea College.
1992, Ph.D., University of Kentucky.
1992-1994, Postdoctoral Scholar, Sanders-Brown Center on Aging, University of Kentucky.

Increasing evidence suggests that alterations in zinc (Zn) homeostasis may contribute to neurodegeneration observed in the pathogenesis of Alzheimer’s disease (AD). Current studies from our laboratory show that there are significant alterations in proteins responsible for the transport of Zn (ZnT proteins) that occur early in the pathogenesis of AD. Our data also suggest that alterations in ZnT proteins and the corresponding disruption of Zn balance can contribute to increased oxidative damage in AD. Our current research centers around the use of Western blot analysis, immunohistochemistry/laser confocal microscopy and genetic manipulation of neuronal cell lines to study alterations of ZnT proteins. We also use GC-MS, HPLC, cell culture techniques, and transgenic animals to correlate altered ZnT levels and markers of oxidative stress including oxidized DNA adducts (8-hydroxyguanine) and neurotoxic byproducts of lipid peroxidation (4-hydroxynonenal).

Representative composite of cells from an MCI subject double labeled for ZnT-6 (A; green) and MC-l (B; red), a marker or early NET formation. Figure C is a merged image. Note considerable overlap between ZnT-6 and MC-1 immunostaining. Scale bar =50 inn.

Visit the Sanders-Brown Center on Aging and its Alzheimer's Disease Research Center.