The Clinical Core (Core B) of the Penn Udall Center has four key functions: 1) To recruit patients with Parkinson's disease (PD), PD with dementia (PDD) dementia with Lewy bodies (DLB), and normal control subjects for the Udall Center's projects;2) To develop strategies for outreach to minorities and recruit them for participation in studies;3) To collaborate with the Administrative and Educational Core (Core A) in educating residents and fellows, health care professionals and the PD community;4) to collaborate with the Statistical Core (Core D) to maintain a secure, compliant, state-of-the-art relational database;and 5) to join with the Neuropathology, Biomarker and Genetics Core (Core C) in collaboration with other Udall Centers on clinical characterization and sample collection. Patients and controls recruited to Core B will consent to donate blood and cerebrospinal fluid (CSF) during life, and brain tissue at death, for the identification of potential biomarkers of PD-related neurodegeneration, including peripheral biochemical analytes and genetic markers in blood and CSF. Participants in the Penn Udall Cohort will have annual evaluations to the time of death. The principal source of patients is the Parkinson's disease and Movement Disorders Center (PD&MDC) of the University of Pennsylvania, located at the Penn Neurological Institute at Pennsylvania Hospital. The PD&MDC is one of the largest referral sites in the northeastern US for the diagnosis and treatment of PD and other movement disorders.
Parkinson's disease (PD) is a common neurodegenerative disease affecting approximately 1 million Americans. While the motor symptoms of PD are well-recognized and can be targeted by effective symptomatic medications, cognitive impairment and dementia in PD are common (affecting 80% of patients with PD for 20 years), costly, and without effective symptomatic therapies. Core B is essential to the success of the Projects of this application and to all collaborations described herein between the Penn Udall Center and other Udall Centers. Thus, Core B is the central clearing house for research that might lead to more meaningful therapies for cognitive impairment in PD.
|Kalia, Lorraine V; Lang, Anthony E; Hazrati, Lili-Naz et al. (2015) Clinical correlations with Lewy body pathology in LRRK2-related Parkinson disease. JAMA Neurol 72:100-5|
|Swanson, Christine R; Li, Katherine; Unger, Travis L et al. (2015) Lower plasma apolipoprotein A1 levels are found in Parkinson's disease and associate with apolipoprotein A1 genotype. Mov Disord 30:805-12|
|Irwin, David J; McMillan, Corey T; Suh, EunRan et al. (2014) Myelin oligodendrocyte basic protein and prognosis in behavioral-variant frontotemporal dementia. Neurology 83:502-9|
|Luk, Kelvin C; Lee, Virginia M-Y (2014) Modeling Lewy pathology propagation in Parkinson's disease. Parkinsonism Relat Disord 20 Suppl 1:S85-7|
|Avants, Brian B; Libon, David J; Rascovsky, Katya et al. (2014) Sparse canonical correlation analysis relates network-level atrophy to multivariate cognitive measures in a neurodegenerative population. Neuroimage 84:698-711|
|Peelle, Jonathan E; Powers, John; Cook, Philip A et al. (2014) Frontotemporal neural systems supporting semantic processing in Alzheimer's disease. Cogn Affect Behav Neurosci 14:37-48|
|Cook, Philip A; McMillan, Corey T; Avants, Brian B et al. (2014) Relating brain anatomy and cognitive ability using a multivariate multimodal framework. Neuroimage 99:477-86|
|Ash, Sharon; Menaged, Anna; Olm, Christopher et al. (2014) Narrative discourse deficits in amyotrophic lateral sclerosis. Neurology 83:520-8|
|McCluskey, Leo; Vandriel, Shannon; Elman, Lauren et al. (2014) ALS-Plus syndrome: non-pyramidal features in a large ALS cohort. J Neurol Sci 345:118-24|
|Escobar, Valerie Drews; Kuo, Yien-Ming; Orrison, Bonnie M et al. (2014) Transgenic mice expressing S129 phosphorylation mutations in ?-synuclein. Neurosci Lett 563:96-100|
Showing the most recent 10 out of 105 publications