The overall goal of the Genetics, Biomarkers, and Neuropathology Core is to provide resources and expertise to PANUC investigators and other collaborators. This Core will: 1. GENETICS;Provide expert preparation of plasma and DNA from Clinical Core participant blood samples. DNA will be stored and used for genetic analysis by Project 3. Blood samples will be appropriately deposited with the NINDS Genetic Resource Center at the Coriell Institute for distribution to other investigators while insuring proper safeguards. 2. BIOMARKER;Provide analysis of CSF using validated biomarkers, and provide a platform for rapid translation of potential new biomarkers for cognitive impairment in Parkinson's disease discovered in a linked ROI AG033398 (Zhang's project) and Project 3. Plasma obtained in Aim 1 will also be stored as a resource for future biomarker studies. 3. NEUROPATHOLOGY: Provide diagnostic expertise to the Clinical Core by providing family members of the deceased and physicians involved in their care with timely autopsy reports based on the most current standardized diagnostic criteria, and optimally prepare brain donations to advance research in Project 2 and Zhang's project. This Core sen/es several initiatives in the NIH Blueprint. It uses existing NIH resources, contributes essential materials to NIH repositories, and is highly patient-oriented and translational

Public Health Relevance

This core will provide support for genetic, biomarker, and neuropathology activities within the Pacific Northwest Udall Center. Biomarkers validated in the Core will be important in aiding the diagnosis of cognitive impairment in patients with Parkinson's disease (PD) as well as monitoring progression and evaluating effectiveness of therapeutics.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Specialized Center (P50)
Project #
5P50NS062684-04
Application #
8382345
Study Section
National Institute of Neurological Disorders and Stroke Initial Review Group (NSD)
Project Start
Project End
Budget Start
2012-08-01
Budget End
2013-07-31
Support Year
4
Fiscal Year
2012
Total Cost
$163,987
Indirect Cost
$61,943
Name
University of Washington
Department
Type
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195
Smulders, Katrijn; Dale, Marian L; Carlson-Kuhta, Patricia et al. (2016) Pharmacological treatment in Parkinson's disease: Effects on gait. Parkinsonism Relat Disord 31:3-13
Wang, Liyong; Maldonado, Lizmarie; Beecham, Gary W et al. (2016) DNA variants in CACNA1C modify Parkinson disease risk only when vitamin D level is deficient. Neurol Genet 2:e72
Mata, Ignacio F; Leverenz, James B; Weintraub, Daniel et al. (2016) GBA Variants are associated with a distinct pattern of cognitive deficits in Parkinson's disease. Mov Disord 31:95-102
Mata, Ignacio F; Davis, Marie Y; Lopez, Alexis N et al. (2016) The discovery of LRRK2 p.R1441S, a novel mutation for Parkinson's disease, adds to the complexity of a mutational hotspot. Am J Med Genet B Neuropsychiatr Genet 171:925-30
Costa-Mallen, Paola; Zabetian, Cyrus P; Hu, Shu-Ching et al. (2016) Smoking and haptoglobin phenotype modulate serum ferritin and haptoglobin levels in Parkinson disease. J Neural Transm (Vienna) 123:1319-1330
Moelter, Stephen T; Weintraub, Daniel; Mace, Lauren et al. (2016) Research consent capacity varies with executive function and memory in Parkinson's disease. Mov Disord 31:414-7
Cholerton, Brenna; Larson, Eric B; Quinn, Joseph F et al. (2016) Precision Medicine: Clarity for the Complexity of Dementia. Am J Pathol 186:500-6
Davis, Marie Y; Johnson, Catherine O; Leverenz, James B et al. (2016) Association of GBA Mutations and the E326K Polymorphism With Motor and Cognitive Progression in Parkinson Disease. JAMA Neurol 73:1217-1224
Costa-Mallen, Paola; Zabetian, Cyrus P; Agarwal, Pinky et al. (2016) Response to the letter "Haptoglobin phenotype and Parkinson disease risk" by Delanghe et al. Parkinsonism Relat Disord 22:110-1
Crane, Paul K; Gibbons, Laura E; Dams-O'Connor, Kristen et al. (2016) Association of Traumatic Brain Injury With Late-Life Neurodegenerative Conditions and Neuropathologic Findings. JAMA Neurol 73:1062-9

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