The Administrative Core's major function is to provide leadership and facilitate the research aims of all cores and projects of the program project with the long-term objective being to learn more about the role of beta amyloid peptide and oxidative damage in the pathogenesis of Alzheimer's disease. The goal of these efforts is to develop knowledge that will lead to the prevention or slowing of AD. This core will promote integration of the cores and projects and facilitate communication between cores and projects by organizing monthly scientific meetings of all investigators and staff. It will provide supervision of all fiscal matters including a monthly financial report to each core and project leader. Scientific and administrative review of the program project will be provided by an Internal Advisory Committee organized by this core. In addition, an External Advisory Committee, composed of scientists with expertise that matches the individual projects, will be named and organized by this core. It will meet annually. These two advisory committees will provide scientific review of accomplishments and future directions of the program project. Another important function of this core is acting as a liaison between the University of Kentucky's Alzheimer's Disease Center and the program project to obtain clinical and neuropathological data and specimens from normal control subjects, preclinical AD subjects, and patients with mild cognitive impairment, late Alzheimer's disease, and frontotemporal dementia (disease control). The Administrative Core provides statistical support for all cores and projects including consultation on research design, power analysis, and statistical analyses. The Core will also maintain a centralized database for all data from cores and projects.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Program Projects (P01)
Project #
5P01AG005119-24
Application #
8376719
Study Section
Special Emphasis Panel (ZAG1-ZIJ-4)
Project Start
Project End
2014-03-31
Budget Start
2012-04-01
Budget End
2013-03-31
Support Year
24
Fiscal Year
2012
Total Cost
$128,265
Indirect Cost
$64,036
Name
University of Kentucky
Department
Type
DUNS #
939017877
City
Lexington
State
KY
Country
United States
Zip Code
40506
Hartz, Anika M S; Zhong, Yu; Wolf, Andrea et al. (2016) Aβ40 Reduces P-Glycoprotein at the Blood-Brain Barrier through the Ubiquitin-Proteasome Pathway. J Neurosci 36:1930-41
Ellison, Elizabeth M; Abner, Erin L; Lovell, Mark A (2016) Multiregional analysis of global 5-methylcytosine and 5-hydroxymethylcytosine throughout the progression of Alzheimer's disease. J Neurochem :
Butterfield, D Allan; Palmieri, Erika M; Castegna, Alessandra (2016) Clinical implications from proteomic studies in neurodegenerative diseases: lessons from mitochondrial proteins. Expert Rev Proteomics 13:259-74
Lovell, Mark A; Abner, Erin; Kryscio, Richard et al. (2015) Calcium Channel Blockers, Progression to Dementia, and Effects on Amyloid Beta Peptide Production. Oxid Med Cell Longev 2015:787805
Sethi, M; Joshi, S S; Webb, R L et al. (2015) Increased fragmentation of sleep-wake cycles in the 5XFAD mouse model of Alzheimer's disease. Neuroscience 290:80-9
Barone, Eugenio; Cenini, Giovanna; Di Domenico, Fabio et al. (2015) Basal brain oxidative and nitrative stress levels are finely regulated by the interplay between superoxide dismutase 2 and p53. J Neurosci Res 93:1728-39
Chen, Chun-Hau; Li, Wenzong; Sultana, Rukhsana et al. (2015) Pin1 cysteine-113 oxidation inhibits its catalytic activity and cellular function in Alzheimer's disease. Neurobiol Dis 76:13-23
Bradley-Whitman, Melissa A; Lovell, Mark A (2015) Biomarkers of lipid peroxidation in Alzheimer disease (AD): an update. Arch Toxicol 89:1035-44
Di Domenico, Fabio; Pupo, Gilda; Mancuso, Cesare et al. (2015) Bach1 overexpression in Down syndrome correlates with the alteration of the HO-1/BVR-a system: insights for transition to Alzheimer's disease. J Alzheimers Dis 44:1107-20
Perluigi, Marzia; Pupo, Gilda; Tramutola, Antonella et al. (2014) Neuropathological role of PI3K/Akt/mTOR axis in Down syndrome brain. Biochim Biophys Acta 1842:1144-53

Showing the most recent 10 out of 238 publications