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Articles by Holly Soares
Total Records ( 7 ) for Holly Soares
  Alex E. Roher , Chera L. Esh , Tyler A. Kokjohn , Eduardo M. Castano , Gregory D. Van Vickle , Walter M. Kalback , R. Lyle Patton , Dean C. Luehrs , Ian D. Daugs , Yu-Min Kuo , Mark R. Emmerling , Holly Soares , Joseph F. Quinn , Jeffrey Kaye , Donald J. Connor , Nina B. Silverberg , Charles H. Adler , James D. Seward , Thomas G. Beach and Marwan N. Sabbagh
>We evaluated the amounts of amyloid beta (Aβ)) peptides in the central nervous system (CNS) and in reservoirs outside the CNS and their potential impact on Aβ plasma levels and Alzheimer`s disease (AD) pathology.
Amyloid β levels were measured in (1) the plasma of AD and nondemented (ND) controls in a longitudinal study, (2) the plasma of a cohort of AD patients receiving a cholinesterase inhibitor, and (3) the skeletal muscle, liver, aorta, platelets, leptomeningeal arteries, and in gray and white matter of AD and ND control subjects.
Plasma Aβ levels fluctuated over time and among individuals, suggesting continuous contributions from brain and peripheral tissues and associations with reactive circulating proteins. Arteries with atherosclerosis had larger amounts of Aβ40 than disease-free vessels. Inactivated platelets contained more Aβ peptides than activated ones. Substantially more Aβ was present in liver samples from ND patients. Overall, AD brain and skeletal muscle contained increased levels of Aβ.
Efforts to use plasma levels of Aβ peptides as AD biomarkers or disease-staging scales have failed. Peripheral tissues might contribute to both the circulating amyloid pool and AD pathology within the brain and its vasculature. The wide spread of plasma Aβ values is also due in part to the ability of Aβ to bind to a variety of plasma and membrane proteins. Sources outside the CNS must be accounted for because pharmacologic interventions to reduce cerebral amyloid are assessed by monitoring Aβ plasma levels. Furthermore, the long-range impact of Aβ immunotherapy on peripheral Aβ sources should also be considered.
  John Q. Trojanowski , Hugo Vandeerstichele , Magdalena Korecka , Christopher M. Clark , Paul S. Aisen , Ronald C. Petersen , Kaj Blennow , Holly Soares , Adam Simon , Piotr Lewczuk , Robert Dean , Eric Siemers , William Z. Potter , Michael W. Weiner , Clifford R. Jack Jr. , William Jagust , Arthur W. Toga , Virginia M.-Y. Lee and Leslie M. Shaw
  Here, we review progress by the Penn Biomarker Core in the Alzheimer's Disease Neuroimaging Initiative (ADNI) toward developing a pathological cerebrospinal fluid (CSF) and plasma biomarker signature for mild Alzheimer's disease (AD) as well as a biomarker profile that predicts conversion of mild cognitive impairment (MCI) and/or normal control subjects to AD. The Penn Biomarker Core also collaborated with other ADNI Cores to integrate data across ADNI to temporally order changes in clinical measures, imaging data, and chemical biomarkers that serve as mileposts and predictors of the conversion of normal control to MCI as well as MCI to AD, and the progression of AD. Initial CSF studies by the ADNI Biomarker Core revealed a pathological CSF biomarker signature of AD defined by the combination of Aβ1-42 and total tau (T-tau) that effectively delineates mild AD in the large multisite prospective clinical investigation conducted in ADNI. This signature appears to predict conversion from MCI to AD. Data fusion efforts across ADNI Cores generated a model for the temporal ordering of AD biomarkers which suggests that Aβ amyloid biomarkers become abnormal first, followed by changes in neurodegenerative biomarkers (CSF tau, F-18 fluorodeoxyglucose-positron emission tomography, magnetic resonance imaging) with the onset of clinical symptoms. The timing of these changes varies in individual patients due to genetic and environmental factors that increase or decrease an individual's resilience in response to progressive accumulations of AD pathologies. Further studies in ADNI will refine this model and render the biomarkers studied in ADNI more applicable to routine diagnosis and to clinical trials of disease modifying therapies.
  Michael W. Weiner , Paul S. Aisen , Clifford R. Jack Jr. , William J. Jagust , John Q. Trojanowski , Leslie Shaw , Andrew J. Saykin , John C. Morris , Nigel Cairns , Laurel A. Beckett , Arthur Toga , Robert Green , Sarah Walter , Holly Soares , Peter Snyder , Eric Siemers , William Potter , Patricia E. Cole and Mark Schmidt
  The Alzheimer’s Disease Neuroimaging Initiative (ADNI) beginning in October 2004, is a 6-year research project that studies changes of cognition, function, brain structure and function, and biomarkers in elderly controls, subjects with mild cognitive impairment, and subjects with Alzheimer’s disease (AD). A major goal is to determine and validate MRI, PET images, and cerebrospinal fluid (CSF)/blood biomarkers as predictors and outcomes for use in clinical trials of AD treatments. Structural MRI, FDG PET, C-11 Pittsburgh compound B (PIB) PET, CSF measurements of amyloid β (Aβ) and species of tau, with clinical/cognitive measurements were performed on elderly controls, subjects with mild cognitive impairment, and subjects with AD. Structural MRI shows high rates of brain atrophy, and has high statistical power for determining treatment effects. FDG PET, C-11 Pittsburgh compound B PET, and CSF measurements of Aβ and tau were significant predictors of cognitive decline and brain atrophy. All data are available at UCLA/LONI/ADNI, without embargo. ADNI-like projects started in Australia, Europe, Japan, and Korea. ADNI provides significant new information concerning the progression of AD.
  Mark E. Schmidt , Eric Siemers , Peter J. Snyder , William Z. Potter , Patricia Cole and Holly Soares
  The Industry Scientific Advisory Board (ISAB) consists of representatives from the private companies and nonprofit foundations participating as sponsors of Alzheimer’s Disease Neuroimaging Initiative (ADNI). Currently 21 companies are represented including pharmaceutical, imaging, and biotech concerns, and two foundations including the Alzheimer’s Association. ISAB members meet regularly by teleconference or face-to-face at ADNI meetings and participate in the ADNI Core groups, all administered and organized by the Foundation for the National Institutes of Health. ISAB ‘deliverables’ include dissemination of information to sponsors, assisting in scientific review of protocols and results, initiation and consideration of “add-on” studies and analyses, and generation of consensus positions on industry priorities and concerns. Although positioned as an advisory body, ISAB also actively contributes to the ADNI mission of identifying biomarkers of disease progression.
  Kaori Ito , Brian Corrigan , Brian Corrigan , Jonathan French , Raymond Miller , Holly Soares , Elyse Katz , Timothy Nicholas , Bill Billing , Richard Anziano and Terence Fullerton
  Background A mathematical model was developed to describe the longitudinal response in Alzheimer's Disease Assessment Scale-cognitive (ADAS-cog) obtained from the Alzheimer's Disease Neuroimaging Initiative. Methods The model was fit to the longitudinal ADAS-cog scores from 817 patients. Risk factors (age, apolipoprotein ɛ4 [APOE ɛ4] genotype, gender, family history of AD, years of education) and baseline severity were tested as covariates. Results Rate of disease progression increased with baseline severity. Age, APOE ɛ4 genotype, and gender were identified as potential covariates influencing disease progression. The rate of disease progression in patients with mild to moderate AD was estimated as approximately 5.5 points/yr. Conclusions A disease progression model adequately described the natural decline of ADAS-cog observed in Alzheimer's Disease Neuroimaging Initiative. Baseline severity is an important covariate to predict a curvilinear rate of disease progression in normal elderly, mild cognitive impairment, and AD patients. Age, APOE ɛ4 genotype, and gender also influence the rate of disease progression.
  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.
  Maria C. Carrillo , Kaj Blennow , Holly Soares , Piotr Lewczuk , Niklas Mattsson , Pankaj Oberoi , Robert Umek , Manu Vandijck , Salvatore Salamone , Tobias Bittner , Leslie M. Shaw , Diane Stephenson , Lisa Bain and Henrik Zetterberg
  Recognizing that international collaboration is critical for the acceleration of biomarker standardization efforts and the efficient development of improved diagnosis and therapy, the Alzheimer's Association created the Global Biomarkers Standardization Consortium (GBSC) in 2010. The consortium brings together representatives of academic centers, industry, and the regulatory community with the common goal of developing internationally accepted common reference standards and reference methods for the assessment of cerebrospinal fluid (CSF) amyloid β42 (Aβ42) and tau biomarkers. Such standards are essential to ensure that analytical measurements are reproducible and consistent across multiple laboratories and across multiple kit manufacturers. Analytical harmonization for CSF Aβ42 and tau will help reduce confusion in the AD community regarding the absolute values associated with the clinical interpretation of CSF biomarker results and enable worldwide comparison of CSF biomarker results across AD clinical studies.
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