archive-org.com » ORG » S » SCIENCEMAG.ORG

Total: 698

Choose link from "Titles, links and description words view":

Or switch to "Titles and links view".

  • 150ra122 VI 4 IP 150 4099 http stm sciencemag org content 4 150 150ra122 short 4100 http stm sciencemag org content 4 150 150ra122 full AB Aggregation of β amyloid Aβ in the brain begins to occur years before the clinical onset of Alzheimer s disease AD Before Aβ aggregation concentrations of extracellular soluble Aβ in the interstitial fluid ISF space of the brain which are regulated by neuronal activity and the sleep wake cycle correlate with the amount of Aβ deposition in the brain seen later The amount and quality of sleep decline with normal aging and to a greater extent in AD patients How sleep quality as well as the diurnal fluctuation in Aβ change with age and Aβ aggregation is not well understood We report a normal sleep wake cycle and diurnal fluctuation in ISF Aβ in the brain of the APPswe PS1δE9 mouse model of AD before Aβ plaque formation After plaque formation the sleep wake cycle markedly deteriorated and diurnal fluctuation of ISF Aβ dissipated As in mice diurnal fluctuation of cerebrospinal fluid Aβ in young adult humans with presenilin mutations was also markedly attenuated after Aβ plaque formation Virtual elimination of Aβ deposits in

    Original URL path: http://stm.sciencemag.org/highwire/citation/186438/medlars (2016-02-10)
    Open archived version from archive


  • the Advancement of Science VO 4 IS 150 SP 150ra122 OP 150ra122 DO 10 1126 scitranslmed 3004291 UL http stm sciencemag org content 4 150 150ra122 abstract AB Aggregation of β amyloid Aβ in the brain begins to occur years before the clinical onset of Alzheimer s disease AD Before Aβ aggregation concentrations of extracellular soluble Aβ in the interstitial fluid ISF space of the brain which are regulated by neuronal activity and the sleep wake cycle correlate with the amount of Aβ deposition in the brain seen later The amount and quality of sleep decline with normal aging and to a greater extent in AD patients How sleep quality as well as the diurnal fluctuation in Aβ change with age and Aβ aggregation is not well understood We report a normal sleep wake cycle and diurnal fluctuation in ISF Aβ in the brain of the APPswe PS1δE9 mouse model of AD before Aβ plaque formation After plaque formation the sleep wake cycle markedly deteriorated and diurnal fluctuation of ISF Aβ dissipated As in mice diurnal fluctuation of cerebrospinal fluid Aβ in young adult humans with presenilin mutations was also markedly attenuated after Aβ plaque formation Virtual elimination of Aβ

    Original URL path: http://stm.sciencemag.org/highwire/citation/186438/refworks (2016-02-10)
    Open archived version from archive

  • Changes in Amyloid-β and Tau in the Cerebrospinal Fluid of Transgenic Mice Overexpressing Amyloid Precursor Protein | Science Translational Medicine
    Staufenbiel Novartis Institutes for Biomedical Research Neuroscience Discovery Basel CH 4056 Basel Switzerland Find this author on Google Scholar Find this author on PubMed Search for this author on this site Mathias Jucker Department of Cellular Neurology Hertie Institute for Clinical Brain Research University of Tübingen D 72076 Tübingen Germany German Center for Neurodegenerative Diseases DZNE D 72076 Tübingen Germany Find this author on Google Scholar Find this author on PubMed Search for this author on this site Article Figures Data Info Metrics eLetters PDF You are currently viewing the abstract View Full Text As a service to the community AAAS Science has made this article free with registration Username Enter your Sciencemag org username Password Enter the password that accompanies your username Forgot your username or password Log in Register for Free Join Subscribe Recommend a subscription to your library Help for librarians Abstract Altered concentrations of amyloid β Aβ peptide and Tau protein in the cerebrospinal fluid CSF are thought to be predictive markers for Alzheimer s disease AD Transgenic mice overexpressing human amyloid precursor protein APP have been used to model Aβ pathology but concomitant changes in Aβ and Tau in CSF have been less well studied We measured Aβ and Tau in the brains and CSF of two well characterized transgenic mouse models of AD one expressing human APP carrying the Swedish mutation APP23 and the other expressing mutant human APP and mutant human presenilin 1 APPPS1 Both mouse models exhibit Aβ deposition in the brain but with different onset and progression trajectories We found an age related 50 to 80 decrease in Aβ42 peptide in mouse CSF and a smaller decrease in Aβ40 both inversely correlated with the brain Aβ load Surprisingly the same mice showed a threefold increase in total endogenous murine Tau in CSF at the stages when Aβ pathology became prominent The results mirror the temporal sequence and magnitude of Aβ and Tau changes in the CSF of patients with sporadic and dominantly inherited AD This observation indicates that APP transgenic mice may be useful as a translational tool for predicting changes in Aβ and Tau markers in the CSF of AD patients These findings also suggest that APP transgenic mouse models may be useful in the search for new disease markers for AD Copyright 2013 American Association for the Advancement of Science View Full Text Science Translational Medicine Vol 5 Issue 194 17 July 2013 Table of Contents Article Tools Email Thank you for your interest in spreading the word about Science Translational Medicine NOTE We only request your email address so that the person you are recommending the page to knows that you wanted them to see it and that it is not junk mail We do not capture any email address Your Email Your Name Send To Enter multiple addresses on separate lines or separate them with commas You are going to email the following Changes in Amyloid β and Tau in the Cerebrospinal Fluid of Transgenic Mice Overexpressing

    Original URL path: http://stm.sciencemag.org/content/5/194/194re2 (2016-02-10)
    Open archived version from archive

  • Clinical trials for neurodevelopmental disorders: At a therapeutic frontier | Science Translational Medicine
    author on Google Scholar Find this author on PubMed Search for this author on this site Article Figures Data Info Metrics eLetters PDF You are currently viewing the View Full Text Username Enter your Sciencemag org username Password Enter the password that accompanies your username Forgot your username or password Log in Join Subscribe Purchase Article Activate Member Account Renew Subscription Recommend a subscription to your library Help for librarians Science Translational Medicine Vol 8 Issue 321 13 January 2016 Table of Contents Article Tools Email Thank you for your interest in spreading the word about Science Translational Medicine NOTE We only request your email address so that the person you are recommending the page to knows that you wanted them to see it and that it is not junk mail We do not capture any email address Your Email Your Name Send To Enter multiple addresses on separate lines or separate them with commas You are going to email the following Clinical trials for neurodevelopmental disorders At a therapeutic frontier Message Subject Your Name has forwarded a page to you from Science Translational Medicine Message Body Your Name thought you would like to see this page from the Science Translational Medicine web site Your Personal Message Send Message Download Powerpoint Print Save to my folders User Name Password Remember my user name password Submit Alerts Please log in to add an alert for this article Username Enter your Sciencemag org username Password Enter the password that accompanies your username Log in Request Permissions Citation tools Clinical trials for neurodevelopmental disorders At a therapeutic frontier By Shafali S Jeste Daniel H Geschwind Science Translational Medicine 13 Jan 2016 321fs1 A well powered clinical trial that failed to replicate promising results in animal models of fragile X syndrome yields important lessons

    Original URL path: http://stm.sciencemag.org/content/8/321/321fs1.figures-only (2016-02-10)
    Open archived version from archive

  • Clinical trials for neurodevelopmental disorders: At a therapeutic frontier | Science Translational Medicine
    1946 6234 Online ISSN 1946 6242 History Copyright Usage Copyright 2016 American Association for the Advancement of Science Author Information Shafali S Jeste 1 and Daniel H Geschwind 2 1 Center for Autism Research and Treatment Semel Institute David Geffen School of Medicine University of California at Los Angeles UCLA Los Angeles CA 90095 17610 USA 2 Center for Autism Research and Treatment Semel Institute and Neurogenetics Program Department of Neurology David Geffen School of Medicine UCLA Los Angeles CA 90095 1761 USA Corresponding author E mail dhg at mednet ucla edu D H G AltMetrics No Altmetric data available for this article Article usage Abstract Full PDF Jan 2016 2727 355 385 Feb 2016 157 42 40 View Full Text Science Translational Medicine Vol 8 Issue 321 13 January 2016 Table of Contents Article Tools Email Thank you for your interest in spreading the word about Science Translational Medicine NOTE We only request your email address so that the person you are recommending the page to knows that you wanted them to see it and that it is not junk mail We do not capture any email address Your Email Your Name Send To Enter multiple addresses on separate lines or separate them with commas You are going to email the following Clinical trials for neurodevelopmental disorders At a therapeutic frontier Message Subject Your Name has forwarded a page to you from Science Translational Medicine Message Body Your Name thought you would like to see this page from the Science Translational Medicine web site Your Personal Message Send Message Download Powerpoint Print Save to my folders User Name Password Remember my user name password Submit Alerts Please log in to add an alert for this article Username Enter your Sciencemag org username Password Enter the password that accompanies your

    Original URL path: http://stm.sciencemag.org/content/8/321/321fs1.article-info (2016-02-10)
    Open archived version from archive

  • Clinical trials for neurodevelopmental disorders: At a therapeutic frontier | Science Translational Medicine
    Center for Autism Research and Treatment Semel Institute and Neurogenetics Program Department of Neurology David Geffen School of Medicine UCLA Los Angeles CA 90095 1761 USA Find this author on Google Scholar Find this author on PubMed Search for this author on this site Article Figures Data Info Metrics eLetters PDF Submit a Response to This Article Compose eLetter Title Contents More information about text formats Plain text Plain text No HTML tags allowed Web page addresses and e mail addresses turn into links automatically Lines and paragraphs break automatically Upload Tables and Figures Attach tables e g doc and figures jpg gif tif by choosing the desired file and then uploading them below Add a new file Upload Files must be less than 100 MB Allowed file types doc jpg jpeg gif tif pdf File names can only contain the following characters A Z a z 0 9 Author Information Contributors First name and middle name First or given name e g Peter Last Name Your last or family name e g MacMoody Email Your email address e g higgs boson gmail com Role Occupation Your role and or occupation e g Orthopedic Surgeon Affiliation Your organization or institution if applicable e g Royal Free Hospital Add another contributor optional Statement of Competing Interests Competing interests Yes No Please describe the competing interests Highwire Comment Subject Apath Vertical Tabs Submit No eLetters have been published for this article View Full Text Science Translational Medicine Vol 8 Issue 321 13 January 2016 Table of Contents Article Tools Email Thank you for your interest in spreading the word about Science Translational Medicine NOTE We only request your email address so that the person you are recommending the page to knows that you wanted them to see it and that it is not junk mail We do not capture any email address Your Email Your Name Send To Enter multiple addresses on separate lines or separate them with commas You are going to email the following Clinical trials for neurodevelopmental disorders At a therapeutic frontier Message Subject Your Name has forwarded a page to you from Science Translational Medicine Message Body Your Name thought you would like to see this page from the Science Translational Medicine web site Your Personal Message Send Message Download Powerpoint Print Save to my folders User Name Password Remember my user name password Submit Alerts Please log in to add an alert for this article Username Enter your Sciencemag org username Password Enter the password that accompanies your username Log in Request Permissions Citation tools Clinical trials for neurodevelopmental disorders At a therapeutic frontier By Shafali S Jeste Daniel H Geschwind Science Translational Medicine 13 Jan 2016 321fs1 A well powered clinical trial that failed to replicate promising results in animal models of fragile X syndrome yields important lessons for clinical trial design Berry Kravis et al this issue Citation Manager Formats BibTeX Bookends EasyBib EndNote tagged EndNote 8 xml Medlars Mendeley Papers RefWorks Tagged Ref Manager

    Original URL path: http://stm.sciencemag.org/content/8/321/321fs1.e-letters (2016-02-10)
    Open archived version from archive

  • Clinical trials for neurodevelopmental disorders: At a therapeutic frontier | Science Translational Medicine
    on this site Article Figures Data Info Metrics eLetters PDF Log in to view full text Username Enter your Sciencemag org username Password Enter the password that accompanies your username Forgot your username or password Log in Join Subscribe Purchase Article Activate Member Account Renew Subscription Recommend a subscription to your library Help for librarians Science Translational Medicine Vol 8 Issue 321 13 January 2016 Table of Contents Article Tools Email Thank you for your interest in spreading the word about Science Translational Medicine NOTE We only request your email address so that the person you are recommending the page to knows that you wanted them to see it and that it is not junk mail We do not capture any email address Your Email Your Name Send To Enter multiple addresses on separate lines or separate them with commas You are going to email the following Clinical trials for neurodevelopmental disorders At a therapeutic frontier Message Subject Your Name has forwarded a page to you from Science Translational Medicine Message Body Your Name thought you would like to see this page from the Science Translational Medicine web site Your Personal Message Send Message Download Powerpoint Print Save to my folders User Name Password Remember my user name password Submit Alerts Please log in to add an alert for this article Username Enter your Sciencemag org username Password Enter the password that accompanies your username Log in Request Permissions Citation tools Clinical trials for neurodevelopmental disorders At a therapeutic frontier By Shafali S Jeste Daniel H Geschwind Science Translational Medicine 13 Jan 2016 321fs1 A well powered clinical trial that failed to replicate promising results in animal models of fragile X syndrome yields important lessons for clinical trial design Berry Kravis et al this issue Citation Manager Formats BibTeX Bookends

    Original URL path: http://stm.sciencemag.org/content/8/321/321fs1.full (2016-02-10)
    Open archived version from archive

  • Table of Contents — January 13, 2016, 8 (321) | Science Translational Medicine
    Articles Mavoglurant in fragile X syndrome Results of two randomized double blind placebo controlled trials By Elizabeth Berry Kravis Vincent Des Portes Randi Hagerman Sébastien Jacquemont Perrine Charles Jeannie Visootsak Marc Brinkman Karin Rerat Barbara Koumaras Liansheng Zhu Gottfried Maria Barth Thomas Jaecklin George Apostol Florian von Raison Science Translational Medicine 13 Jan 2016 321ra5 In contrast to previous studies targeting the mGluR pathway in fragile X syndrome patients did not improve behavior independent of FMR1 methylation Editor s Summary Abstract Full Text PDF Repetitive blast exposure in mice and combat veterans causes persistent cerebellar dysfunction By James S Meabon Bertrand R Huber Donna J Cross Todd L Richards Satoshi Minoshima Kathleen F Pagulayan Ge Li Kole D Meeker Brian C Kraemer Eric C Petrie Murray A Raskind Elaine R Peskind David G Cook Science Translational Medicine 13 Jan 2016 321ra6 Ventral regions of the cerebellum in combat veterans and mice are vulnerable to long term traumatic brain injury caused by repetitive blast exposure Editor s Summary Abstract Full Text PDF Inhibition of diacylglycerol kinase α restores restimulation induced cell death and reduces immunopathology in XLP 1 By Elisa Ruffo Valeria Malacarne Sasha E Larsen Rupali Das Laura Patrussi Christoph Wülfing Christoph Biskup Senta M Kapnick Katherine Verbist Paige Tedrick Pamela L Schwartzberg Cosima T Baldari Ignacio Rubio Kim E Nichols Andrew L Snow Gianluca Baldanzi Andrea Graziani Science Translational Medicine 13 Jan 2016 321ra7 DGKα inhibition restores apoptosis in SAP deficient lymphocytes decreasing immunopathology in XLP 1 patients Editor s Summary Abstract Full Text PDF Cord blood monocyte derived inflammatory cytokines suppress IL 2 and induce nonclassic T H 2 type immunity associated with development of food allergy By Yuxia Zhang Fiona Collier Gaetano Naselli Richard Saffery Mimi LK Tang Katrina J Allen Anne Louise Ponsonby Leonard C Harrison Peter Vuillermin on behalf of the BIS Investigator Group Science Translational Medicine 13 Jan 2016 321ra8 Infants who develop food allergy display hyperresponsive innate immunity at birth that promotes nonclassical T H 2 differentiation Editor s Summary Abstract Full Text PDF Editors Choice Cancer care looks ROSEy By Marshaleen Henriques Forsythe Science Translational Medicine 13 Jan 2016 321ec5 Rapid on site evaluation ROSE potentially enhances bronchoscopic methods for lung cancer genotyping Full Text Clocking in to the brain s activity By Yo El Ju Science Translational Medicine 13 Jan 2016 321ec6 Aging alters the circadian rhythmicity of gene expression in the human brain Full Text Noncoding RNA plugs into a proinflammatory circuit By Alexander Marson Science Translational Medicine 13 Jan 2016 321ec7 Rmrp a long noncoding RNA and DDX5 an RNA helicase are potential therapeutic targets for autoimmunity Full Text An integrative analysis sheds light on methylation profiles By Masako Suzuki Science Translational Medicine 13 Jan 2016 321ec8 Genetic influence is not negligible for testing DNA methylation profiles in human studies Full Text Erratum Erratum for the Research Article CMV specific T cells generated from naïve T cells recognize atypical epitopes and may be protective in vivo by P J

    Original URL path: http://stm.sciencemag.org/content/8/321.toc (2016-02-10)
    Open archived version from archive



  •