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Articles by Ronald C. Petersen
Total Records ( 3 ) for Ronald C. Petersen
  Danielle C. Whitehair , Abdullah Sherzai , Jennifer Emond , Rema Raman , Paul S. Aisen , Ronald C. Petersen and Adam S. Fleisher
  Background: Apolipoprotein E ε4 (APOE ε4) allele carrier status has been well established as a risk factor for developing Alzheimer's disease. However, the specific influence of APOE ε4 allele status on cognitive and functional rates of decline in mild cognitive impairment (MCI) is poorly understood. We examine the prospective association of APOE ε4 allele status on measures of cognitive and functional decline in subjects with amnestic MCI (aMCI). Methods: A total of 516 aMCI participants aged 55–90 years who received placebo or vitamin E from the Alzheimer's Disease Cooperative Study's MCI treatment trial were evaluated. During the 36-month study period, neurocognitive and functional measures were collected. These measures were assessed over time for change and association with APOE ε4 status. Generalized Estimating Equations were performed to model each outcome measure over the study period. Results: APOE ε4 status had a significant impact on cognitive and functional decline on multiple measures; those who were APOE ε4 positive had significantly more rapid decline in performance on all cognitive and functional measures except Number Cancellation and Maze tracing (P < .05). The greatest decline was seen in global measures of cognition and function including the Clinical Diagnostic Rating scale, followed by the Mini-Mental State Examination, Global Deterioration scale, and the Alzheimer's Disease Assessment Scale-Cognitive Subscale. Conclusions: These findings demonstrate that APOE ε4 genotype is predictive of increased general rates of decline with global measures of cognition and function most affected. With accelerated declines in common clinical trial primary efficacy measures, APOE ε4 status needs to be accounted for in treatment trials of MCI.
  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.
  Paul S. Aisen , Ronald C. Petersen , Michael C. Donohue , Anthony Gamst , Rema Raman , Ronald G. Thomas , Sarah Walter , John Q. Trojanowski , Leslie M. Shaw , Laurel A. Beckett , Clifford R. Jack Jr. , William Jagust , Arthur W. Toga , Andrew J. Saykin , John C. Morris , Robert C. Green and Michael W. Weiner
  The Clinical Core of the Alzheimer’s Disease Neuroimaging Initiative (ADNI) has provided clinical, operational, and data management support to ADNI since its inception. This article reviews the activities and accomplishments of the core in support of ADNI aims. These include the enrollment and follow-up of more than 800 subjects in the three original cohorts: healthy controls, amnestic mild cognitive impairment (now referred to as late MCI, or LMCI), and mild Alzheimer’s disease (AD) in the first phase of ADNI (ADNI 1), with baseline longitudinal, clinical, and cognitive assessments. These data, when combined with genetic, neuroimaging, and cerebrospinal fluid measures, have provided important insights into the neurobiology of the AD spectrum. Furthermore, these data have facilitated the development of novel clinical trial designs. ADNI has recently been extended with funding from an NIH Grand Opportunities (GO) award, and the new ADNI GO phase has been launched; this includes the enrollment of a new cohort, called early MCI, with milder episodic memory impairment than the LMCI group. An application for a further 5 years of ADNI funding (ADNI 2) was recently submitted. This funding would support ongoing follow-up of the original ADNI 1 and ADNI GO cohorts, as well as additional recruitment into all categories. The resulting data would provide valuable data on the earliest stages of AD, and support the development of interventions in these critically important populations.
 
 
 
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