OVERALL ABSTRACT The Northwestern ADC is in its 21st year. This proposal aims to establish an Imaging Core to address an unmet need for the Northwestern Alzheimer?s Disease Center (ADC). In this ?Overall? component of the application, the specific aims, innovation and approach sections will address the impact of the revision on the entire Northwestern ADC. The section on the proposed Imaging Core will address these aspects from the focused vantage point of imaging methodology, infrastructure and scientific content. Nearly all of these Specific Aims will be enhanced by the availability of the Imaging Core. The proposed Core will extend the mission and mandate of the ADC by: ? Improving the characterization and diagnostic classification of Clinical Core subjects; ? Adding quantitative and uniformly standardized imaging-based biomarker information (e.g., atrophy, blood flow, connectivity, amyloid, tau, etc.) to the data entered into NACC modules; ? Unburdening researchers using Clinical Core subjects from the need to gather ad hoc imaging data; ? Increasing the range of hypotheses that can be addressed by collaborative projects relying on Northwestern ADC resources (e.g., collaborators can request cognitively healthy controls with or without elevated amyloid PET to address their hypotheses) Specific examples are provided in the letters of support; ? Adding a new dimension to clinicopathologic investigations of autopsy specimens (e.g., what is the relationship between atrophy measured by MR imaging and the number of neurons, microglia, neurofibrillary tangles?).
The Northwestern ADC is part of a national network of AD Centers funded by the NIA, which contains resources and researchers aiming to discover the causes and treatments of AD and related dementias. The current application proposes to add an Imaging Core in order to obtain state-of-the-art brain in vivo quantitative brain imaging, which is becoming increasingly more important for identifying people at risk for Alzheimer?s disease, for making an accurate dementia diagnosis, and for ascertaining the effectiveness of interventions.
|Alosco, Michael L; Duskin, Jonathan; Besser, Lilah M et al. (2017) Modeling the Relationships Among Late-Life Body Mass Index, Cerebrovascular Disease, and Alzheimer's Disease Neuropathology in an Autopsy Sample of 1,421 Subjects from the National Alzheimer's Coordinating Center Data Set. J Alzheimers Dis 57:953-968|
|Pandya, Seema Y; Lacritz, Laura H; Weiner, Myron F et al. (2017) Predictors of Reversion from Mild Cognitive Impairment to Normal Cognition. Dement Geriatr Cogn Disord 43:204-214|
|Jun, Gyungah R; Chung, Jaeyoon; Mez, Jesse et al. (2017) Transethnic genome-wide scan identifies novel Alzheimer's disease loci. Alzheimers Dement 13:727-738|
|Jutkowitz, Eric; MacLehose, Richard F; Gaugler, Joseph E et al. (2017) Risk Factors Associated With Cognitive, Functional, and Behavioral Trajectories of Newly Diagnosed Dementia Patients. J Gerontol A Biol Sci Med Sci 72:251-258|
|Katsumata, Yuriko; Nelson, Peter T; Ellingson, Sally R et al. (2017) Gene-based association study of genes linked to hippocampal sclerosis of aging neuropathology: GRN, TMEM106B, ABCC9, and KCNMB2. Neurobiol Aging 53:193.e17-193.e25|
|Yu, Xiao-Wen; Curlik, Daniel M; Oh, M Matthew et al. (2017) CREB overexpression in dorsal CA1 ameliorates long-term memory deficits in aged rats. Elife 6:|
|Ward, Michael E; Chen, Robert; Huang, Hsin-Yi et al. (2017) Individuals with progranulin haploinsufficiency exhibit features of neuronal ceroid lipofuscinosis. Sci Transl Med 9:|
|Jefferson-George, Kyra S; Wolk, David A; Lee, Edward B et al. (2017) Cognitive decline associated with pathological burden in primary age-related tauopathy. Alzheimers Dement 13:1048-1053|
|Morhardt, Darby J; O'Hara, Mary C; Zachrich, Kristine et al. (2017) Development of a psycho-educational support program for individuals with primary progressive aphasia and their care-partners. Dementia (London) :1471301217699675|
|Mackenzie, Ian R; Nicholson, Alexandra M; Sarkar, Mohona et al. (2017) TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics. Neuron 95:808-816.e9|
Showing the most recent 10 out of 383 publications