The Administrative and Clinical Core administers the MSA PPG. The Principal investigator (PI) is Dr. Low, who will be assisted by Dr. Sid Gilman (Co-PI), who will have a specific focus on administering the Clinical Core.
The specific aims of Core A are to: 1. Provide supervision and direction for the program project as a whole. 2. Maintain appropriate policies and procedures and manuals as required and ensure that all instruments, such as the Unified Multiple System Atrophy Rating Scale (UMSARS), COMPASS, and COMPASS-change are current. 3. Coordinate the conference calls and meetings of the Steering Committee and the conference calls and meetings of Scientific Advisory Committee (SAC). 4. Provide fiscal control for the operations of the program project, including establishment and maintenance of subcontracts and making payments to projects, cores, and enrolling investigators. 5. Monitor recruitment, the timely transfer of data from sites to the Data Core (Core B), the provision of blood samples to the Genetics Core (Core D), interaction of enrolling sites with Project 1 (Gilman), and the transfer of autopsy samples to the Neuropathology Core (Core C) and Project 2 (Benarroch). 6. Liaison with NINDS and provide performance reports to the Performance and Safety Monitoring Board (PSMB) and liaison with the European MSA study Group. A key function is the integration of activities of the 3 cores and 4 projects by facilitating the flow of information between areas. This function has evolved to a high level over the past 4 years and will be further enhanced. Core A will also facilitate interactions with the Steering Committee and Advisory Board. 7. The Clinical Core houses the double-blind placebo controlled study to evaluate if Rifampicin will halt or reverse progression of neurological and autonomic deficits in eariy cases of MSA. This study is housed in this core to emphasize the important core nature of the study, since it brings together the activities of Projects 1, 3, and 4. 8. Liason with Autonomic Rare Disease Research Consortium (U54 NS065736) in the implementation and supervision of the Rifampicin study.
Multiple system atrophy (MSA) is a progressive and fatal disease. Its cause is unknown and treatment is unsatisfactory. This Program Project is specifically devoted to MSA and focuses on the improved diagnosis, improved understanding of its natural history, and an understanding of what causes the disease. This Core administers the PPG and houses an important treatment trial aimed at halting the progression of the disease.
|Singer, Wolfgang; Berini, Sarah E; Sandroni, Paola et al. (2017) Pure autonomic failure: Predictors of conversion to clinical CNS involvement. Neurology 88:1129-1136|
|Valera, Elvira; Spencer, Brian; Mott, Jennifer et al. (2017) MicroRNA-101 Modulates Autophagy and Oligodendroglial Alpha-Synuclein Accumulation in Multiple System Atrophy. Front Mol Neurosci 10:329|
|Coon, Elizabeth A; Low, Phillip A (2017) Pure autonomic failure without alpha-synuclein pathology: an evolving understanding of a heterogeneous disease. Clin Auton Res 27:67-68|
|Valera, Elvira; Spencer, Brian; Fields, Jerel A et al. (2017) Combination of alpha-synuclein immunotherapy with anti-inflammatory treatment in a transgenic mouse model of multiple system atrophy. Acta Neuropathol Commun 5:2|
|Spencer, Brian; Valera, Elvira; Rockenstein, Edward et al. (2017) Anti-?-synuclein immunotherapy reduces ?-synuclein propagation in the axon and degeneration in a combined viral vector and transgenic model of synucleinopathy. Acta Neuropathol Commun 5:7|
|Coon, Elizabeth A; Fealey, Robert D; Sletten, David M et al. (2017) Anhidrosis in multiple system atrophy involves pre- and postganglionic sudomotor dysfunction. Mov Disord 32:397-404|
|Coon, Elizabeth A; Ahlskog, J Eric; Silber, Michael H et al. (2017) Do selective serotonin reuptake inhibitors improve survival in multiple system atrophy? Parkinsonism Relat Disord :|
|Spencer, Brian; Kim, Changyoun; Gonzalez, Tania et al. (2016) ?-Synuclein interferes with the ESCRT-III complex contributing to the pathogenesis of Lewy body disease. Hum Mol Genet 25:1100-15|
|Loavenbruck, Adam J; Singer, Wolfgang; Mauermann, Michelle L et al. (2016) Transthyretin amyloid neuropathy has earlier neural involvement but better prognosis than primary amyloid counterpart: an answer to the paradox? Ann Neurol 80:401-11|
|Spencer, Brian; Williams, Stephanie; Rockenstein, Edward et al. (2016) ?-synuclein conformational antibodies fused to penetratin are effective in models of Lewy body disease. Ann Clin Transl Neurol 3:588-606|
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