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Articles by Marwan Sabbagh
Total Records ( 2 ) for Marwan Sabbagh
  Zaven S. Khachaturian , Deborah Barnes , Richard Einstein , Sterling Johnson , Virginia Lee , Allen Roses , Mark A. Sager , William R. Shankle , Peter J. Snyder , Ronald C. Petersen , Gerard Schellenberg , John Trojanowski , Paul Aisen , Marilyn S. Albert , John C.S. Breitner , Neil Buckholtz , Maria Carrillo , Steven Ferris , Barry D. Greenberg , Michael Grundman , Ara S. Khachaturian , Lewis H. Kuller , Oscar L. Lopez , Paul Maruff , Richard C. Mohs , Marcelle Morrison- Bogorad , Creighton Phelps , Eric Reiman , Marwan Sabbagh , Mary Sano , Lon S. Schneider , Eric Siemers , Pierre Tariot , Jacques Touchon , Bruno Vellas and Lisa J. Bain
  Among the major impediments to the design of clinical trials for the prevention of Alzheimer's disease (AD), the most critical is the lack of validated biomarkers, assessment tools, and algorithms that would facilitate identification of asymptomatic individuals with elevated risk who might be recruited as study volunteers. Thus, the Leon Thal Symposium 2009 (LTS'09), on October 27–28, 2009 in Las Vegas, Nevada, was convened to explore strategies to surmount the barriers in designing a multisite, comparative study to evaluate and validate various approaches for detecting and selecting asymptomatic people at risk for cognitive disorders/dementia. The deliberations of LTS'09 included presentations and reviews of different approaches (algorithms, biomarkers, or measures) for identifying asymptomatic individuals at elevated risk for AD who would be candidates for longitudinal or prevention studies. The key nested recommendations of LTS'09 included: (1) establishment of a National Database for Longitudinal Studies as a shared research core resource; (2) launch of a large collaborative study that will compare multiple screening approaches and biomarkers to determine the best method for identifying asymptomatic people at risk for AD; (3) initiation of a Global Database that extends the concept of the National Database for Longitudinal Studies for longitudinal studies beyond the United States; and (4) development of an educational campaign that will address public misconceptions about AD and promote healthy brain aging.
  John C. Breitner , Laura D. Baker , Thomas J. Montine , Curtis L. Meinert , Constantine G. Lyketsos , Karen H. Ashe , Jason Brandt , Suzanne Craft , Denis E. Evans , Robert C. Green , M. Saleem Ismail , Barbara K. Martin , Michael J. Mullan , Marwan Sabbagh and Pierre N. Tariot
  Background Epidemiologic evidence suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) delay onset of Alzheimer‘s dementia (AD), but randomized trials show no benefit from NSAIDs in patients with symptomatic AD. The Alzheimer‘s Disease Anti-inflammatory Prevention Trial (ADAPT) randomized 2528 elderly persons to naproxen or celecoxib versus placebo for 2 years (standard deviation = 11 months) before treatments were terminated. During the treatment interval, 32 cases of AD revealed increased rates in both NSAID-assigned groups. Methods We continued the double-masked ADAPT protocol for 2 additional years to investigate incidence of AD (primary outcome). We then collected cerebrospinal fluid (CSF) from 117 volunteer participants to assess their ratio of CSF tau to Aβ1-42. Results Including 40 new events observed during follow-up of 2071 randomized individuals (92% of participants at treatment cessation), there were 72 AD cases. Overall, NSAID-related harm was no longer evident, but secondary analyses showed that increased risk remained notable in the first 2.5 years of observations, especially in 54 persons enrolled with cognitive impairment––no dementia (CIND). These same analyses showed later reduction in AD incidence among asymptomatic enrollees who were given naproxen. CSF biomarker assays suggested that the latter result reflected reduced Alzheimer-type neurodegeneration. Conclusions These data suggest a revision of the original ADAPT hypothesis that NSAIDs reduce AD risk, as follows: NSAIDs have an adverse effect in later stages of AD pathogenesis, whereas asymptomatic individuals treated with conventional NSAIDs such as naproxen experience reduced AD incidence, but only after 2 to 3 years. Thus, treatment effects differ at various stages of disease. This hypothesis is consistent with data from both trials and epidemiological studies.
 
 
 
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