The primary mission of Core A is to provide leadership, coordination and integration of all the components of the UK-ADC, so that our programmatic and scientific goals are achieved. Our overall scientific objective is to support and facilitate research aimed at elucidating the pathogenic mechanisms underlying the transitions from normal cognitive aging to the development of AD, with a long-term goal of enabling more effective translation of this mechanistic knowledge to intervention strategies. The UK-ADC has historically been at the forefront of supporting research in identification of the early manifestations of disease and the pathogenic mechanisms underlying the transitions from normal cognitive aging to the development of AD. In the renewal period, we will build upon this highly successful focus, as well as leverage several recent positive developments at UK that will expand our translational research capability, and thereby help to increase the rate of progress toward new therapies to delay or prevent AD. The UK-ADC functions in a multidisciplinary, integrated, and supportive environment that catalyzes high-quality AD research within the UK community and throughout Kentucky and beyond. The ADC also enhances education and outreach within UK and in the community, and provides clinical diagnoses and care of patients with cognitive impairment. The ADC serves as the focal point of all AD-related activities in Kentucky, providing the infrastructure and resources to enhance scientific interactions and develop new collaborations. The ADC also reaches beyond Kentucky to enhance AD research, education, and clinical practice on a national level through its interactions with other ADCs, as well as other regional and national institutions, including the Alzheimer's Association, NIA and industry. An effective Administrative Core is essential for transforming ADC goals into accomplishments. Therefore, Core A will continue to support the ability of our UK-ADC to serve as a critical resource for the university, community, state, region and nation through a set of integrated and intertwined specific aims.
Aim 1 : Provide leadership and an organizational framework for management and coordination of all ADC activities to ensure optimal resource utilization to meet the overall goals of the ADC.
Aim 2 : Enable the ADC to serve as the focal point of AD-related activities in Kentucky by continuing to coordinate, facilitate, and promote scientific interactions.
Aim 3 : Contribute to and interact with other ADCs and other national collaborative activities and the lay community, to increase visibility of the ADC and maximize progress in AD research throughout the country.
Our goal is to catalyze outstanding AD research while ensuring more rapid progress toward new therapies to delay or prevent AD, so that our human volunteers, patients and caregivers become the beneficiaries of our advances in knowledge. Our well integrated center is moving the field of cognitive aging and AD forward and supporting the elucidation of mechanisms of disease progression so that successful interventions can be developed in the future to treat or prevent this most dehumanizing disorder to affect humans.
|Perez, Sylvia E; He, Bin; Nadeem, Muhammad et al. (2015) Resilience of precuneus neurotrophic signaling pathways despite amyloid pathology in prodromal Alzheimer's disease. Biol Psychiatry 77:693-703|
|Segerstrom, Suzanne C; Eisenlohr-Moul, Tory A; Evans, Daniel R et al. (2015) Repetitive thought dimensions, psychological well-being, and perceived growth in older adults: a multilevel, prospective study. Anxiety Stress Coping 28:287-302|
|Powell, David; Caban-Holt, Allison; Jicha, Gregory et al. (2014) Frontal white matter integrity in adults with Down syndrome with and without dementia. Neurobiol Aging 35:1562-9|
|Brenowitz, Willa D; Monsell, Sarah E; Schmitt, Frederick A et al. (2014) Hippocampal sclerosis of aging is a key Alzheimer's disease mimic: clinical-pathologic correlations and comparisons with both alzheimer's disease and non-tauopathic frontotemporal lobar degeneration. J Alzheimers Dis 39:691-702|
|Nelson, Peter T; Estus, Steven; Abner, Erin L et al. (2014) ABCC9 gene polymorphism is associated with hippocampal sclerosis of aging pathology. Acta Neuropathol 127:825-43|
|Matveev, Sergey V; Spielmann, Hans Peter; Metts, Brittney M et al. (2014) A distinct subfraction of A? is responsible for the high-affinity Pittsburgh compound B-binding site in Alzheimer's disease brain. J Neurochem 131:356-68|
|Weekman, Erica M; Sudduth, Tiffany L; Abner, Erin L et al. (2014) Transition from an M1 to a mixed neuroinflammatory phenotype increases amyloid deposition in APP/PS1 transgenic mice. J Neuroinflammation 11:127|
|Parikh, Ishita; Medway, Christopher; Younkin, Steven et al. (2014) An intronic PICALM polymorphism, rs588076, is associated with allelic expression of a PICALM isoform. Mol Neurodegener 9:32|
|Bradley-Whitman, Melissa A; Timmons, Michael D; Beckett, Tina L et al. (2014) Nucleic acid oxidation: an early feature of Alzheimer's disease. J Neurochem 128:294-304|
|Kryscio, Richard J; Abner, Erin L; Cooper, Gregory E et al. (2014) Self-reported memory complaints: implications from a longitudinal cohort with autopsies. Neurology 83:1359-65|
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