Abstract

Core C: The Transgenic and Neurobehavior Core has three major aims:
Specific Aim #1 : To generate and maintain breeding colonies of transgenic and gene-targeted mouse lines and to provide cohorts of transgenic and gene-targeted mice for studies proposed in Projects #1 to #3 of the Center grant.
Specific Aim #2 : To establish C57BL/6 cogenic lines of the transgenic and gene-targeted mice used throughout the study.
Specific Aim #3 : To establish methods to examine behavioral motor and clinical deficits in mouse models of Parkinson's disease. Core C: The Transgenic and neurobehavior core will be a shared central resource of the Parkinson's Disease Research Center servicing Projects 1, 2, and 3 and will play a central role in our investigations in the pathogenesis of Parkinson's disease.

Public Health Relevance

Through the development and maintenance of new and existing mouse models of PD and the neurobehavioral analysis of these PD models, this core will provide the basis for transgenic technology and phenotypic analysis of mice as a central resource to all three projects in the Center to support their research into the pathogenesis of PD.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Specialized Center (P50)
Project #
5P50NS038377-15
Application #
8533023
Study Section
National Institute of Neurological Disorders and Stroke Initial Review Group (NSD)
Project Start
Project End
Budget Start
2013-08-01
Budget End
2014-07-31
Support Year
15
Fiscal Year
2013
Total Cost
$149,879
Indirect Cost
$58,489

  Institution

Name
Johns Hopkins University
Department
Type
DUNS #
001910777
City
Baltimore
State
MD
Country
United States
Zip Code
21218

  Publications

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
Dawson, Ted M; Golde, Todd E; Lagier-Tourenne, Clotilde (2018) Animal models of neurodegenerative diseases. Nat Neurosci 21:1370-1379
Lee, Saebom; Kim, Sangjune; Park, Yong Joo et al. (2018) The c-Abl inhibitor, Radotinib HCl, is neuroprotective in a preclinical Parkinson's disease mouse model. Hum Mol Genet 27:2344-2356
Xiong, Yulan; Neifert, Stewart; Karuppagounder, Senthilkumar S et al. (2018) Robust kinase- and age-dependent dopaminergic and norepinephrine neurodegeneration in LRRK2 G2019S transgenic mice. Proc Natl Acad Sci U S A 115:1635-1640
Yun, Seung Pil; Kam, Tae-In; Panicker, Nikhil et al. (2018) Block of A1 astrocyte conversion by microglia is neuroprotective in models of Parkinson's disease. Nat Med 24:931-938

Showing the most recent 10 out of 250 publications