Abstract

The Clinical Core seeks to improve the diagnosis and management of individuals with Parkinson disease (PD) through its support of the JHU Udall Center and Clinical Project 3. With this funding period request, the Clinical Core will add biofluid ascertainment (blood, urine, and cerebrospinal fluid (CSF)) to its existing 15-year longitudinal study and brain autopsy program. Through the collection of biofluids from individuals who undergo autopsy the Clinical Core is uniquely situated to allow the Clinical Project to identify PD biomarkers. In addition, to ensure that the Clinical Project has sufficient CSF to complete its aims, the Clinical Core will be responsible for obtaining CSF through collaborations with other cohorts both within and outside JHU. The Clinical Core also seeks to fulfill the mission of the JHU Udall Center through its efforts to educate patients, their families, and health care providers regarding the Center's research activities, PD diagnosis and treatment.

Public Health Relevance

The Clinical Core will be a shared resource of the Parkinson's Disease Research Center and will play a central role in our investigations in the pathogenesis of Parkinson's Disease. The Clinical Core will provide vital support to the Clinical Project 3 through its acquisition of cerebrospinal fluid. It will also support the missions of the other cores and projects through its longitudinal investigation and brain autopsy program as well as education initiatives.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Specialized Center (P50)
Project #
5P50NS038377-20
Application #
9551705
Study Section
Special Emphasis Panel (ZNS1)
Project Start
Project End
Budget Start
2018-08-01
Budget End
2019-07-31
Support Year
20
Fiscal Year
2018
Total Cost
Indirect Cost

  Institution

Name
Johns Hopkins University
Department
Type
DUNS #
001910777
City
Baltimore
State
MD
Country
United States
Zip Code
21205

  Publications

Kim, Sangjune; Yun, Seung Pil; Lee, Saebom et al. (2018) GBA1 deficiency negatively affects physiological ?-synuclein tetramers and related multimers. Proc Natl Acad Sci U S A 115:798-803
Kim, Donghoon; Yoo, Je Min; Hwang, Heehong et al. (2018) Graphene quantum dots prevent ?-synucleinopathy in Parkinson's disease. Nat Nanotechnol :
Hinkle, Jared T; Perepezko, Kate; Mari, Zoltan et al. (2018) Perceived Treatment Status of Fluctuations in Parkinson Disease Impacts Suicidality. Am J Geriatr Psychiatry 26:700-710
Kaji, Seiji; Maki, Takakuni; Kinoshita, Hisanori et al. (2018) Pathological Endogenous ?-Synuclein Accumulation in Oligodendrocyte Precursor Cells Potentially Induces Inclusions in Multiple System Atrophy. Stem Cell Reports 10:356-365
Yun, Seung Pil; Kim, Donghoon; Kim, Sangjune et al. (2018) ?-Synuclein accumulation and GBA deficiency due to L444P GBA mutation contributes to MPTP-induced parkinsonism. Mol Neurodegener 13:1
Hinkle, Jared T; Perepezko, Kate; Rosenthal, Liana S et al. (2018) Markers of impaired motor and cognitive volition in Parkinson's disease: Correlates of dopamine dysregulation syndrome, impulse control disorder, and dyskinesias. Parkinsonism Relat Disord 47:50-56
Berger, Nathan A; Besson, Valerie C; Boulares, A Hamid et al. (2018) Opportunities for the repurposing of PARP inhibitors for the therapy of non-oncological diseases. Br J Pharmacol 175:192-222
Wu, Xinyan; Zahari, Muhammad Saddiq; Renuse, Santosh et al. (2018) Quantitative phosphoproteomic analysis reveals reciprocal activation of receptor tyrosine kinases between cancer epithelial cells and stromal fibroblasts. Clin Proteomics 15:21
Blauwendraat, Cornelis; Pletnikova, Olga; Geiger, Joshua T et al. (2018) Genetic analysis of neurodegenerative diseases in a pathology cohort. Neurobiol Aging :
Heo, Seok; Diering, Graham H; Na, Chan Hyun et al. (2018) Identification of long-lived synaptic proteins by proteomic analysis of synaptosome protein turnover. Proc Natl Acad Sci U S A 115:E3827-E3836

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