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作 者:Kelsie M.LaBarbera Yvette I.Sheline Nicholas J.Izzo Carla M.Yuede Lora Waybright Raymond Yurko Hannah M.Edwards Woodrow D.Gardiner Kaj Blennow Henrik Zetterberg Anne Börjesson-Hanson Roger Morgan Charles S.Davis Robert J.Guttendorf Lon S.Schneider Steven DeKosky Harry LeVine III Michael Grundman Anthony O.Caggiano John R.Cirrito Susan M.Catalano Mary E.Hamby
机构地区:[1]Cognition Therapeutics Inc.,Pittsburgh,PA,USA [2]University of Pennsylvania,Philadelphia,USA [3]Washington University,St.Louis,USA [4]University of Gothenburg,Mölndal,Sweden [5]Department of Psychiatry and Neurochemistry,Institute of Neuroscience and Physiology,The Sahlgrenska Academy at the University of Gothenburg,Mölndal,Sweden [6]Clinical Neurochemistry Laboratory,Sahlgrenska University Hospital,Mölndal,Sweden [7]Department of Neurodegenerative Disease,UCL Institute of Neurology,Queen Square,London,UK [8]UK Dementia Research Institute at UCL,London,UK [9]Hong Kong Center for Neurodegenerative Diseases,Clear Water Bay,Hong Kong,China [10]Wisconsin Alzheimer’s Disease Research Center,University of Wisconsin School of Medicine and Public Health,University of Wisconsin-Madison,Madison,WI,USA [11]Karolinska University Hospital,Stockholm,Sweden [12]MedSurgPI,LLC,Raleigh,NC,USA [13]CSD Biostatistics,Inc.,Oro Valley,AZ,USA [14]Aclairo Pharmaceutical Development Group,Inc,Vienna,VA,USA [15]Keck School of Medicine of USC,Los Angeles,CA,USA [16]McKnight Brain Institute,University of Florida,Gainesville,FL,USA [17]Sanders-Brown Center on Aging,University of Kentucky,Lexington,KY,USA [18]Global R&D Partners,LLC,San Diego,CA,USA [19]Department of Neurosciences,University of California,San Diego,USA
出 处:《Translational Neurodegeneration》2023年第1期568-571,共4页转化神经变性病(英文)
基 金:supported by grants from the National Institute on Aging(AG057780 to SMC)and by Cognition Therapeutics,Inc.
摘 要:Trial Registration:May 11th,2018 ClinicalTrials.gov Identifier:NCT03522129 https://clini caltr ials.gov/ct2/show/NCT03522129.Investigational therapies for Alzheimer’s disease(AD)target a wide range of mechanisms,yet promising dis-ease-modifying therapies remain a huge unmet need.Much evidence indicates that the oligomeric form of amyloid-beta(Aβ)is a toxic species contributing to AD through synaptic damage and neuronal toxicity[1].
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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