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Articles by Kurt R. Brunden
Total Records ( 3 ) for Kurt R. Brunden
  Shaohua Xu , Kurt R. Brunden , John Q. Trojanowski and Virginia M.-Y. Lee
  Background The assembly of tau proteins into paired helical filaments, the building blocks of neurofibrillary tangles, is linked to neurodegeneration in Alzheimer's disease and related tauopathies. A greater understanding of this assembly process could identify targets for the discovery of drugs to treat Alzheimer's disease and related disorders. By using recombinant human tau, we have delineated events leading to the conversion of normal soluble tau into tau fibrils. Methods Atomic force microscopy and transmission electron microscopy methodologies were used to determine the structure of tau assemblies that formed when soluble tau was incubated with heparin for increasing lengths of time. Results Tau initially oligomerizes into spherical nucleation units of 18- to 21-nm diameter that appear to assemble linearly into nascent fibrils. Among the earliest tau fibrils are species that resemble a string of beads formed by linearly aligned spheres that with time seem to coalesce to form straight and twisted ribbon-like filaments, as well as paired helical filaments similar to those found in human tauopathies. An analysis of fibril cross sections at later incubation times revealed three fundamental axial structural features. Conclusions By monitoring tau fibrillization, we showed that different tau filament morphologies coexist. Temporal changes in the predominant tau structural species suggest that tau fibrillization involves the generation of structural intermediates, resulting in the formation of tau fibrils with verisimilitude to their authentic human counterparts.
  Mary D. Naylor , Jason H. Karlawish , Steven E. Arnold , Ara S. Khachaturian , Zaven S. Khachaturian , Virginia M.-Y. Lee , Matthew Baumgart , Sube Banerjee , Cornelia Beck , Kaj Blennow , Ron Brookmeyer , Kurt R. Brunden , Kathleen C. Buckwalter , Meryl Comer , Kenneth Covinsky , Lynn Friss Feinberg , Giovanni Frisoni , Colin Green , Renato Maia Guimaraes , Lisa P. Gwyther , Franz F. Hefti , Michael Hutton , Claudia Kawas , David M. Kent , Lewis Kuller , Kenneth M. Langa , Robert W. Mahley , Katie Maslow , Colin L. Masters , Diane E. Meier , Peter J. Neumann , Steven M. Paul , Ronald C. Petersen , Mark A. Sager , Mary Sano , Dale Schenk , Holly Soares , Reisa A. Sperling , Sidney M. Stahl , Vivianna van Deerlin , Yaakov Stern , David Weir , David A. Wolk and John Q. Trojanowski
  To address the pending public health crisis due to Alzheimer‘s disease (AD) and related neurodegenerative disorders, the Marian S. Ware Alzheimer Program at the University of Pennsylvania held a meeting entitled "State of the Science Conference on the Advancement of Alzheimer's Diagnosis, Treatment and Care," on June 21-22, 2012. The meeting comprised four workgroups focusing on Biomarkers; Clinical Care and Health Services Research; Drug Development; and Health Economics, Policy, and Ethics. The workgroups shared, discussed, and compiled an integrated set of priorities, recommendations, and action plans, which are presented in this article.
  John Q. Trojanowski , Steven E. Arnold , Jason H. Karlawish , Mary Naylor , Kurt R. Brunden and Virginia M.-Y. Lee
  The emerging global epidemic of Alzheimer‘s disease (AD) demands novel paradigms to address the two unmet needs of the field: (a) cost-effective health care delivery programs/services, and (b) clinical and basic research to accelerate therapy discovery/development. This report outlines a model demonstration project, the Marian S. Ware Alzheimer Program at the University of Pennsylvania, which was designed to achieve four specific aims: (1) improve the integration and continuity of AD care; (2) identify biomarkers that detect the earliest presence of AD and related neurodegenerative cognitive disorders; (3) enhance both the design and conduct of clinical trials as well as review their results to more effectively test new AD therapies and translate valuable therapies into clinical practice; and (4) discover and develop novel disease-modifying small molecule treatments for AD. The ”Ware-UPenn“ program has been presented in this report as a useful prototype for partnerships between private philanthropy and academia in planning and developing programs to address a major national public health problem.
 
 
 
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