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Articles by Jose L. Molinuevo
Total Records ( 2 ) for Jose L. Molinuevo
  Niklas Mattsson , Ulf Andreasson , Staffan Persson , Maria C. Carrillo , Steven Collins , Sonia Chalbot , Neal Cutler , Diane Dufour- Rainfray , Anne M. Fagan , Niels H.H. Heegaard , Ging-Yuek Robin Hsiung , Bradley Hyman , Khalid Iqbal , D. Richard Lachno , Alberto Lleo , Piotr Lewczuk , Jose L. Molinuevo , Piero Parchi , Axel Regeniter , Robert Rissman , Hanna Rosenmann , Giuseppe Sancesario , Johannes Schroder , Leslie M. Shaw , Charlotte E. Teunissen , John Q. Trojanowski , Hugo Vanderstichele , Manu Vandijck , Marcel M. Verbeek , Henrik Zetterberg , Kaj Blennow and Stephan A. Kaser
  Background The cerebrospinal fluid (CSF) biomarkers amyloid beta 1–42, total tau, and phosphorylated tau are used increasingly for Alzheimer's disease (AD) research and patient management. However, there are large variations in biomarker measurements among and within laboratories. Methods Data from the first nine rounds of the Alzheimer's Association quality control program was used to define the extent and sources of analytical variability. In each round, three CSF samples prepared at the Clinical Neurochemistry Laboratory (Molndal, Sweden) were analyzed by single-analyte enzyme-linked immunosorbent assay (ELISA), a multiplexing xMAP assay, or an immunoassay with electrochemoluminescence detection. Results A total of 84 laboratories participated. Coefficients of variation (CVs) between laboratories were around 20% to 30%; within-run CVs, less than 5% to 10%; and longitudinal within-laboratory CVs, 5% to 19%. Interestingly, longitudinal within-laboratory CV differed between biomarkers at individual laboratories, suggesting that a component of it was assay dependent. Variability between kit lots and between laboratories both had a major influence on amyloid beta 1–42 measurements, but for total tau and phosphorylated tau, between-kit lot effects were much less than between-laboratory effects. Despite the measurement variability, the between-laboratory consistency in classification of samples (using prehoc-derived cutoffs for AD) was high (>90% in 15 of 18 samples for ELISA and in 12 of 18 samples for xMAP). Conclusions The overall variability remains too high to allow assignment of universal biomarker cutoff values for a specific intended use. Each laboratory must ensure longitudinal stability in its measurements and use internally qualified cutoff levels. Further standardization of laboratory procedures and improvement of kit performance will likely increase the usefulness of CSF AD biomarkers for researchers and clinicians.
  Serge Gauthier and Jose L. Molinuevo
  Background Clinical studies and post hoc analyses have investigated the use of combination therapy for the treatment of Alzheimer's disease (AD). We review the evidence for the short- and long-term efficacy of combination therapy in AD. Methods The review is based on a search of the PubMed database to identify relevant articles concerning combination treatment with memantine and cholinesterase inhibitors (ChEIs). Results In patients with moderate–to–severe AD, combination treatment with the N-methyl–d–aspartate receptor antagonist memantine and the ChEI donepezil has produced significant benefits in cognition, function, behavior, global outcome, and care dependency, compared with donepezil treatment alone. Data from long–term observational studies support these findings. Compared with ChEI monotherapy, combination treatment slowed cognitive and functional decline (a 4–year sustained effect that appeared to increase over time) and reduced the risk of nursing home admission. Preclinically, the combination of N–methyl–d–aspartate receptor modulation and acetylcholinesterase inhibition has been shown to act synergistically, which may explain the observed clinical effects of combination treatment. Conclusion Treatment with memantine/ChEI combination therapy in moderate–to–severe AD produces consistent benefits that appear to increase over time, and that are beyond those of ChEI treatment alone.
 
 
 
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