The major objective of the Administration Core is to manage the progress of the Program Project with the ultimate goal of discovering novel mechanisms and drugs which are effective in the therapy of cognitive decline associated with normal aging and AD.
The specific aims of the Administration Core are: 1To hold overall responsibility for the administration of the program project. This goal would be achieved through frequent meetings of the program director with project and core directors, a group of external advisors and an Internal (Heath Science Center-wide) Advisory Committee and with the able assistance of an administrative assistant. 2. To manage the fiscal aspects of the Program Project. The program director will supervise and the administrative assistant will carry out the fiscal aspects of the program of research. 3. To manage the interactions between projects and cores. The design of this program of research requires thoughtful coordination of the interactions of research projects with two essential cores, the Animal Care and Behavioral Assessment Core (Core B) and the Electrophysiology Core (Core C). We will coordinate activities to achieve delivery of behaviorally characterized, aged mice to research projects in a manner that represents our historical population of aged animals as a whole. 4.To coordinate tissue sharing among research projects. Procedures are developed and implemented to ensure that all valuable animals and tissues generated as a result of the activities of this program of research are used or stored. 5. To foster an environment for the intellectual interactions of program investigators and between program investigators and the UNT Health Science Center community. 6. To Provide Biostatistical Support to the Project and Cores. The biostatistics component of this core will continue to conduct power analyses as part of the design of proposed studies, will provide advise to investigators on proposed analytic methods for both planned and post-hoc analyses (univariate or multivariate analyses for group difference) and management of the data that results from the various projects. Finally, the biostatistician will perform analysis of results of our behavioral assessment of mice to insure appropriate distribution of mice to each of the projects. These Adminisition Core functions has served this progress well during the first funding cycle and will continue to do so.
| Izurieta Munoz, Haydee; Gonzales, Eric B; Sumien, Nathalie (2018) Effects of creatine supplementation on nociception in young male and female mice. Pharmacol Rep 70:316-321 |
| Mock, J Thomas; Knight, Sherilynn G; Vann, Philip H et al. (2018) Gait Analyses in Mice: Effects of Age and Glutathione Deficiency. Aging Dis 9:634-646 |
| Grillo, Michael A; Grillo, Stephanie L; Gerdes, Bryan C et al. (2018) Control of Neuronal Ryanodine Receptor-Mediated Calcium Signaling by Calsenilin. Mol Neurobiol : |
| Kaja, Simon; Payne, Andrew J; Naumchuk, Yuliya et al. (2017) Quantification of Lactate Dehydrogenase for Cell Viability Testing Using Cell Lines and Primary Cultured Astrocytes. Curr Protoc Toxicol 72:2.26.1-2.26.10 |
| Shetty, Ritu A; Rutledge, Margaret A; Forster, Michael J (2017) Retrograde conditioning of place preference and motor activity with cocaine in mice. Psychopharmacology (Berl) 234:515-522 |
| Engler-Chiurazzi, E B; Brown, C M; Povroznik, J M et al. (2017) Estrogens as neuroprotectants: Estrogenic actions in the context of cognitive aging and brain injury. Prog Neurobiol 157:188-211 |
| Engler-Chiurazzi, Elizabeth B; Covey, Douglas F; Simpkins, James W (2017) A novel mechanism of non-feminizing estrogens in neuroprotection. Exp Gerontol 94:99-102 |
| Mock, J Thomas; Chaudhari, Kiran; Sidhu, Akram et al. (2017) The influence of vitamins E and C and exercise on brain aging. Exp Gerontol 94:69-72 |
| Engler-Chiurazzi, E B; Singh, M; Simpkins, J W (2016) From the 90's to now: A brief historical perspective on more than two decades of estrogen neuroprotection. Brain Res 1633:96-100 |
| Russell, Ashley E; Doll, Danielle N; Sarkar, Saumyendra N et al. (2016) TNF-? and Beyond: Rapid Mitochondrial Dysfunction Mediates TNF-?-Induced Neurotoxicity. J Clin Cell Immunol 7: |
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