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Articles by Dale Schenk
Total Records ( 3 ) for Dale Schenk
  Maria C. Carrillo , Andrew Blackwell , Harald Hampel , Johan Lindborg , Reisa Sperling , Dale Schenk , Jeffrey J. Sevigny , Steven Ferris , David A. Bennett , Suzanne Craft , Timothy Hsu and William Klunk
  The purpose of the Alzheimer's Association Research Roundtable meeting was to discuss the potential of finding diagnostic tools to determine the earliest risk factors for Alzheimer's disease (AD). Currently, drugs approved for AD address symptoms which are generally manifest after the disease is already well-established, but there is a growing pipeline of drugs that may alter the underlying pathology and therefore slow or halt progression of the disease. As these drugs become available, it will become increasingly imperative that those at risk for AD be detected and possibly treated early, especially given recent indications that the disease process may start decades before the first clinical symptoms are recognized. Early detection must go hand-in-hand with qualified tools to determine the efficacy of drugs in people who may be asymptomatic or who have only very mild symptoms of the disease. Devising strategies and screening tools to identify and monitor those at risk in order to perform ”prevention” trials is seen by many as a top public-health priority, made all the more urgent by an impending growth in the elderly population worldwide.
  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.
  Byron Zhao , Mei Yu , Martin Neitzel , Jennifer Marugg , Jacek Jagodzinski , Mike Lee , Kang Hu , Dale Schenk , Ted Yednock and Guriqbal Basi
  Production of amyloid β peptides (Aβ), followed by their deposition in the brain as amyloid plaques, contributes to the hallmark pathology of Alzheimer disease. The enzymes responsible for production of Aβ, BACE1 and γ-secretase, are therapeutic targets for treatment of Alzheimer disease. Two presenilin (PS) homologues, referred to as PS1 and PS2, comprise the catalytic core of γ-secretase. In comparing presenilin selectivity of several classes of γ-secretase inhibitors, we observed that sulfonamides in general tend to be more selective for inhibition of PS1-comprising γ-secretase, as exemplified by ELN318463 and BMS299897. We employed a combination of chimeric constructs and point mutants to identify structural determinants for PS1-selective inhibition by ELN318463. Our studies identified amino acid residues Leu172, Thr281, and Leu282 in PS1 as necessary for PS1-selective inhibition by ELN318463. These residues also contributed in part to the PS1-selective inhibition by BMS299897. Alanine scanning mutagenesis of areas flanking Leu172, Thr281, and Leu282 identified additional amino acids that affect inhibitor potency of not only these sulfonamides but also nonsulfonamide inhibitors, without affecting Aβ production and presenilin endoproteolysis. Interestingly, many of these same residues have been identified previously to be important for γ-secretase function. These findings implicate TM3 and a second region near the carboxyl terminus of PS1 aminoterminal fragment in mediating the activity of γ-secretase inhibitors. Our observations demonstrate that PS-selective inhibitors of γ-secretase are feasible, and such inhibitors may allow differential inhibition of Aβ peptide production and Notch signaling.

 
 
 
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