The main functions of the Administrative Core are to: a) facilitate distribution of research materials and resources to the various investigators;b) facilitate communication between investigators, cores the advisory committees, affiliated institutions and the funding agency;c) evaluate the quality of ongoing research as well as programs to be considered for future expansion;d) cut brain tissue specimens and harvest frozen specimens for distribution, in a blinded fashion for investigators;d) interact with Core B and e) maintain a web page for the PPG. Core A functions will be accomplished with the help of three different committees: 1) the Internal Advisory group consisting of project and core leaders. It will meet on a monthly basis to discuss research projects, protocols, results and any problems that might arise in this collaborative effort. The External Advisory Committee which consists of scientists with expertise in various disciplines represented in this application will meet with Internal Advisory Committee every other a year. In the off years there will be video conferences. It will review progress and advise on the overall quality of the work. Meeting will be chaired by the Core leader. Dr. Mufson. These meetings will provide a forum for discussing new ideas and a mechanism for expanding the program with worthy projects in the future. The Administrative Core will be led by the Principal Investigator and Co-PL of the Core.
A centralized Administrative Core is a necessity for the daily function of the entire program project since it the PPG brings together investigators from three NIA funded Alzheimer's disease center. The core coordinates budgetary and organization issues as well as transfers and tracks tissue specimens provided for each subproject.
|Tiernan, Chelsea T; Combs, Benjamin; Cox, Kristine et al. (2016) Pseudophosphorylation of tau at S422 enhances SDS-stable dimer formation and impairs both anterograde and retrograde fast axonal transport. Exp Neurol 283:318-29|
|Mufson, Elliott J; Ikonomovic, Milos D; Counts, Scott E et al. (2016) Molecular and cellular pathophysiology of preclinical Alzheimer's disease. Behav Brain Res 311:54-69|
|Rosa, Elyse; Mahendram, Sujeivan; Ke, Yazi D et al. (2016) Tau downregulates BDNF expression in animal and cellular models of Alzheimer's disease. Neurobiol Aging 48:135-142|
|Kirkwood, Caitlin M; MacDonald, Matthew L; Schempf, Tadhg A et al. (2016) Altered Levels of Visinin-Like Protein 1 Correspond to Regional Neuronal Loss in Alzheimer Disease and Frontotemporal Lobar Degeneration. J Neuropathol Exp Neurol 75:175-82|
|Mufson, Elliott J; Malek-Ahmadi, Michael; Snyder, Noelle et al. (2016) Braak stage and trajectory of cognitive decline in noncognitively impaired elders. Neurobiol Aging 43:101-10|
|Strupp, Barbara J; Powers, Brian E; Velazquez, Ramon et al. (2016) Maternal Choline Supplementation: A Potential Prenatal Treatment for Down Syndrome and Alzheimer's Disease. Curr Alzheimer Res 13:97-106|
|Mizukami, Katsuyoshi; Akatsu, Hiroyasu; Abrahamson, Eric E et al. (2016) Immunohistochemical analysis of hippocampal butyrylcholinesterase: Implications for regional vulnerability in Alzheimer's disease. Neuropathology 36:135-45|
|Gorelick, Philip B; Counts, Scott E; Nyenhuis, David (2016) Vascular cognitive impairment and dementia. Biochim Biophys Acta 1862:860-8|
|Tiernan, Chelsea T; Ginsberg, Stephen D; Guillozet-Bongaarts, Angela L et al. (2016) Protein homeostasis gene dysregulation in pretangle-bearing nucleus basalis neurons during the progression of Alzheimer's disease. Neurobiol Aging 42:80-90|
|Beck, John S; Mufson, Elliott J; Counts, Scott E (2016) Evidence for Mitochondrial UPR Gene Activation in Familial and Sporadic Alzheimer's Disease. Curr Alzheimer Res 13:610-4|
Showing the most recent 10 out of 245 publications