Demands on the Clinical Core for clearly defined samples of persons with AD, related dementias, MCI, Lewy body spectrum disease, and age-matched controls have become more complex. Subject samples appropriate for one type of Investigation (e.g., a clinical treatment trial) are often not appropriate for other types of studies (e.g., case-control epidemiologic or genetic linkage analysis studies). Still others are needed for training clinicians to manage the multiple clinical problems expressed during the course of dementia. To meet these demands, the Clinical Core will continue to provide AD patients, non-AD dementia patients, MCI, and cognitively normal subjects selected for maximum appropriateness for participation in clinical studies. We will focus on early AD, MCI, and cognitively normal older controls. In addition, subjects with non-AD neurodegenerative dementing disorders and Lewy body spectrum disease will be recruited and followed. The Clinical Core jointly with the Education and Information Core will recruit African American AD patients, non-AD dementia patients, MCI, and cognitively normal subjects who are willing to participate in the full range of UW ADRC and ADRC-affiliated clinical research. Clinical Core personnel support and interact with population-based cohorts of late life dementia and normal control subjects appropriate for epidemiologic studies and for accession of normal control postmortem brain tissue. We will continue to collect cerebrospinal fluid (CSF), plasma and serum on these subject samples, and through multi-ADC collaborative efforts, continue to expand the UW ADRC CSF bank to support the search for biomarkers for diagnosis, monitoring disease progression, and identifying asymptomatic persons at risk for dementing disorders. Subjects, biological fluid samples, and data will be provided to meet the research needs of ADRC investigators, the broader UW research community, and investigators at other Institutions.

Public Health Relevance

AD remains an impending public health crisis with no very effective treatments, no cure, and no prevention. This application responds to the need for increased knowledge in AD so that effective treatments can be developed.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Specialized Center (P50)
Project #
5P50AG005136-30
Application #
8459473
Study Section
Special Emphasis Panel (ZAG1-ZIJ-4)
Project Start
Project End
Budget Start
2013-05-01
Budget End
2014-04-30
Support Year
30
Fiscal Year
2013
Total Cost
$664,282
Indirect Cost
$71,885
Name
University of Washington
Department
Type
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195
Ridge, Perry G; Hoyt, Kaitlyn B; Boehme, Kevin et al. (2016) Assessment of the genetic variance of late-onset Alzheimer's disease. Neurobiol Aging 41:200.e13-20
Toledo, Jon B; Gopal, Pallavi; Raible, Kevin et al. (2016) Pathological α-synuclein distribution in subjects with coincident Alzheimer's and Lewy body pathology. Acta Neuropathol 131:393-409
Ringman, John M; Monsell, Sarah; Ng, Denise W et al. (2016) Neuropathology of Autosomal Dominant Alzheimer Disease in the National Alzheimer Coordinating Center Database. J Neuropathol Exp Neurol 75:284-90
Brenowitz, Willa D; Hubbard, Rebecca A; Keene, C Dirk et al. (2016) Mixed neuropathologies and estimated rates of clinical progression in a large autopsy sample. Alzheimers Dement :
Besser, Lilah M; Alosco, Michael L; Ramirez Gomez, Liliana et al. (2016) Late-Life Vascular Risk Factors and Alzheimer Disease Neuropathology in Individuals with Normal Cognition. J Neuropathol Exp Neurol 75:955-962
Crane, Paul K; Gibbons, Laura E; McCurry, Susan M et al. (2016) Importance of home study visit capacity in dementia studies. Alzheimers Dement 12:419-26
Burke, Shanna L; Maramaldi, Peter; Cadet, Tamara et al. (2016) Neuropsychiatric symptoms and Apolipoprotein E: Associations with eventual Alzheimer's disease development. Arch Gerontol Geriatr 65:231-8
Beckelman, Brenna C; Zhou, Xueyan; Keene, C Dirk et al. (2016) Impaired Eukaryotic Elongation Factor 1A Expression in Alzheimer's Disease. Neurodegener Dis 16:39-43
Henderson, Benjamin W; Gentry, Erik G; Rush, Travis et al. (2016) Rho-associated protein kinase 1 (ROCK1) is increased in Alzheimer's disease and ROCK1 depletion reduces amyloid-β levels in brain. J Neurochem 138:525-31
Tosto, Giuseppe; Monsell, Sarah E; Hawes, Stephen E et al. (2016) Progression of Extrapyramidal Signs in Alzheimer's Disease: Clinical and Neuropathological Correlates. J Alzheimers Dis 49:1085-93

Showing the most recent 10 out of 583 publications