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 #
5P50NS038377-12
Application #
8132256
Study Section
National Institute of Neurological Disorders and Stroke Initial Review Group (NSD)
Project Start
Project End
Budget Start
2010-08-01
Budget End
2011-07-31
Support Year
12
Fiscal Year
2010
Total Cost
$162,370
Indirect Cost

  Institution

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

  Publications

Hinkle, Jared T; Perepezko, Kate; Mills, Kelly A et al. (2018) Dopamine transporter availability reflects gastrointestinal dysautonomia in early Parkinson disease. Parkinsonism Relat Disord 55:8-14
Kim, Donghoon; Hwang, Heehong; Choi, Seulah et al. (2018) D409H GBA1 mutation accelerates the progression of pathology in A53T ?-synuclein transgenic mouse model. Acta Neuropathol Commun 6:32
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

Showing the most recent 10 out of 250 publications