1989 B.S. Biology, Wake Forest University
1997 PhD Pharmacology, University of Kentucky
Our lab uses cutting edge molecular, electrophysiologic, anatomic and behavioral techniques to study the influence of stress and sleep on aging brain function. We are particularly interested in how these changes may set the stage for age-related vulnerability to neurodegenerative diseases like Alzheimer's and Parkinson's. In collaboration with other laboratories, we are also investigating myelin, vasculature, and glucose utilization-related issues using the aging rodent brain. Our lab also focuses on bioinformatic disciplines related to analysis and integration of large data sets within and across studies.
Psychosocial Stress Interactions with Electrophysiology and Brain Aging
R01AG037868 (Blalock PI, 2 Co-investigators) 03/01/2011 – 02/28/2016
NIH/ NIA $1,517,830 (total)
Investigation of the influence of psychosocial stress on hippocampal function with age, as well as the potential for interventions to modify the effects of stress.
Hippocampal Synaptic Structure - Physiology During Aging (Renewal)
R01 AG004542-22 (Blalock Co-I; Landfield PI) 04/01/2011 – 03/31/2016
The major goals of this project are to investigate the mechanisms underlying altered Ca2+ regulation and impaired neuronal function or neuronal vulnerability with aging. Advanced Ca2+ imaging technology is used concomitantly with electrophysiology in cultures and hippocampal slices.
Hippocampal Electrophysiology and Myelinogenesis in Healthy Cognitive Aging
R01AG034605 (Blalock Co-I, PI Landfield) 09/01/09 – 08/31/14
NIH/NIA $2,993,890 (total)
The goal of this project is to test the novel hypothesis that increased myelinogenesis we have seen in the hippocampus during rodent aging is a major factor in cognitive decline.
Metabolic Syndrome and Hippocampal Calcium Dysregulation in Aging-related Memory Decline
R01AG033649 (Blalock Co-I, PI Thibault) 8/1/09- 7/31/14
NIH/NIA $1,477,375 (total)
This project investigates the role of metabolic syndrome in altered hippocampal Ca2+ homeostasis and tests the hypothesis that these actions are mediated in part by changes in brain insulin/glucose signaling pathways and can be counteracted by anti-diabetic drugs.