The Udall Center for Excellence in Parkinson Disease Research at the Mayo Clinic is an integrated, multi-disciplinary research program focusing on of the "Genetics and Molecular Biology of Parkinsonism." The Udall Center draws upon the clinical strengths of the Mayo Clinic Movement Disorder Section with its longitudinal studies of Parkinson disease (PD) and a focus on the clinical genetics of familial Parkinsonism, a large brain bank of Parkinsonian disorders and strong institutional commitment to PD research and education. All components of the Udall Center are based in Jacksonville, Florida, although core resources in Rochester, Minnesota, particularly the Division of Biomedical Statistics will be used. Mayo Foundation educational resources, including sponsored seminar series and graduate level educational courses on PD and other neurodegenerative disorders are also utilized. The proposal is highly innovative and original in that it addresses the intriguing interaction between two molecules with surprising similarities, tau and a-synuclein, both of which are strongly implicated as critical factors in pathogenesis of parkinsonian disorders. The clinical, genetic and pathologic studies proposed capitalize on inherent strengths of the Udall Center investigators and unique clinical, genetic and pathological resources that have been built over the years due to the fervent devotion of investigators to better understanding PD and related disorders. The Center also brings established investigators in complementary areas of research (Drs. Rademakers and Petrucelli) to the task of understanding how tau is related PD and how tau-directed therapies may translate into novel treatments for PD and parkinsonian tauopathies. The proposed Center will have three projects and four cores with an overarching theme to understand the role of tau in PD and parkinsonian tauopathies. Project 1, entitled "Identification of novel parkinsonian genes by whole-genome sequencing," is led by Rosa Rademakers, PhD. Project 2, entitled "Genetic determinants of a-synuclein and tau pathology in Parkinsonism," is led by Dennis W. Dickson, MD. Project 3, entitled "Identification and testing of novel compounds to treat Parkinsonism," is led by Leonard Petrucelli, PhD. Core A (Administration) and Core D (Neuropathology) are led by Dennis W. Dickson, MD. Core B (Clinical) is led by Zbigniew K. Wszoiek, MD. Core C (Genetics) is led by Owen A. Ross, PhD.
Parkinson disease (PD) is one of the leading causes of neurologic disability. Increasingly, it is recognized that there is a genetic component to risk for PD and related disorders sometimes referred to as Parkinsonism-plus. Research in our Center will find new genes for familial PD and increase our understanding of how common differences in the genetic make-up of individuals leads to sporadic PD. Finally, our research will work towards discovering drugs that can treat PD and Parkinsonism-plus disorders.
|Kertesz, A; Finger, E; Murrell, J et al. (2015) Progressive supranuclear palsy in a family with TDP-43 pathology. Neurocase 21:178-84|
|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|
|Sundal, C; Baker, M; Karrenbauer, V et al. (2015) Hereditary diffuse leukoencephalopathy with spheroids with phenotype of primary progressive multiple sclerosis. Eur J Neurol 22:328-33|
|Fujioka, Shinsuke; Sanchez Contreras, Monica Y; Strongosky, Audrey J et al. (2015) Three sib-pairs of autopsy-confirmed progressive supranuclear palsy. Parkinsonism Relat Disord 21:101-5|
|Bieniek, Kevin F; van Blitterswijk, Marka; Baker, Matthew C et al. (2014) Expanded C9ORF72 hexanucleotide repeat in depressive pseudodementia. JAMA Neurol 71:775-81|
|Bras, Jose; Guerreiro, Rita; Darwent, Lee et al. (2014) Genetic analysis implicates APOE, SNCA and suggests lysosomal dysfunction in the etiology of dementia with Lewy bodies. Hum Mol Genet 23:6139-46|
|Ross, Jay P; Rayaprolu, Sruti; Bernales, Cecily Q et al. (2014) SLC1A2 rs3794087 does not associate with essential tremor. Neurobiol Aging 35:935.e9-10|
|Heckman, Michael G; Elbaz, Alexis; Soto-Ortolaza, Alexandra I et al. (2014) Protective effect of LRRK2 p.R1398H on risk of Parkinson's disease is independent of MAPT and SNCA variants. Neurobiol Aging 35:266.e5-14|
|Angeles, Dario C; Ho, Patrick; Chua, Ling Ling et al. (2014) Thiol peroxidases ameliorate LRRK2 mutant-induced mitochondrial and dopaminergic neuronal degeneration in Drosophila. Hum Mol Genet 23:3157-65|
|Bailey, Rachel M; Howard, John; Knight, Joshua et al. (2014) Effects of the C57BL/6 strain background on tauopathy progression in the rTg4510 mouse model. Mol Neurodegener 9:8|
Showing the most recent 10 out of 127 publications