نتایج جستجو برای: amyloid β

تعداد نتایج: 204360  

2012
Mingmin Yan Shanping Mao Huimin Dong Baohui Liu Qian Zhang Gaofeng Pan Zhiping Fu

PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually in...

Journal: :Alzheimer's & Dementia 2015
Osama Sabri Marwan N. Sabbagh John Seibyl Henryk Barthel Hiroyasu Akatsu Yasuomi Ouchi Kohei Senda Shigeo Murayama Kenji Ishii Masaki Takao Thomas G. Beach Christopher C. Rowe James B. Leverenz Bernardino Ghetti James W. Ironside Ana M. Catafau Andrew W. Stephens Andre Mueller Norman Koglin Anja Hoffmann Katrin Roth Cornelia Reininger Walter J. Schulz-Schaeffer

BACKGROUND Evaluation of brain β-amyloid by positron emission tomography (PET) imaging can assist in the diagnosis of Alzheimer disease (AD) and other dementias. METHODS Open-label, nonrandomized, multicenter, phase 3 study to validate the (18)F-labeled β-amyloid tracer florbetaben by comparing in vivo PET imaging with post-mortem histopathology. RESULTS Brain images and tissue from 74 dece...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2014
Willem Huijbers Elizabeth C Mormino Sarah E Wigman Andrew M Ward Patrizia Vannini Donald G McLaren J Alex Becker Aaron P Schultz Trey Hedden Keith A Johnson Reisa A Sperling

Normal aging is often difficult to distinguish from the earliest stages of Alzheimer's disease. Years before clinical memory deficits manifest, amyloid-β deposits in the cortex in many older individuals. Neuroimaging studies indicate that a set of densely connected neocortical regions, referred to as the default network, is especially vulnerable to amyloid-β deposition. Yet, the impact of amylo...

2017
Fan Liao Hyejin Yoon Jungsu Kim

PURPOSE OF REVIEW APOE4 genotype is the strongest genetic risk factor for Alzheimer's disease. Prevailing evidence suggests that amyloid β plays a critical role in Alzheimer's disease. The objective of this article is to review the recent findings about the metabolism of apolipoprotein E (ApoE) and amyloid β and other possible mechanisms by which ApoE contributes to the pathogenesis of Alzheime...

Journal: :Brain : a journal of neurology 2016
Aurélien Lathuilière Vanessa Laversenne Alberto Astolfo Erhard Kopetzki Helmut Jacobsen Marco Stampanoni Bernd Bohrmann Bernard L Schneider Patrick Aebischer

Passive immunization against misfolded toxic proteins is a promising approach to treat neurodegenerative disorders. For effective immunotherapy against Alzheimer's disease, recent clinical data indicate that monoclonal antibodies directed against the amyloid-β peptide should be administered before the onset of symptoms associated with irreversible brain damage. It is therefore critical to devel...

Journal: :Brain : a journal of neurology 2011
Dun-Sheng Yang Philip Stavrides Panaiyur S Mohan Susmita Kaushik Asok Kumar Masuo Ohno Stephen D Schmidt Daniel Wesson Urmi Bandyopadhyay Ying Jiang Monika Pawlik Corrinne M Peterhoff Austin J Yang Donald A Wilson Peter St George-Hyslop David Westaway Paul M Mathews Efrat Levy Ana M Cuervo Ralph A Nixon

Autophagy, a major degradative pathway for proteins and organelles, is essential for survival of mature neurons. Extensive autophagic-lysosomal pathology in Alzheimer's disease brain contributes to Alzheimer's disease pathogenesis, although the underlying mechanisms are not well understood. Here, we identified and characterized marked intraneuronal amyloid-β peptide/amyloid and lysosomal system...

2015
Matthew A. Barrett Richard J. Alsop Thomas Hauß Maikel C. Rheinstädter Shiro Suetsugu

Amyloid-β peptides interact with cell membranes in the human brain and are associated with neurodegenerative diseases, such as Alzheimer's disease. An emerging explanation of the molecular mechanism, which results in neurodegeneration, places the cause of neurotoxicity of the amyloid- peptides on their potentially negative interaction with neuronal membranes. It is known that amyloid-β peptides...

2017
Sinwoo Hwang Joo Weon Lim Hyeyoung Kim

Alzheimer's disease (AD) is a fatal neurodegenerative disease. Brain amyloid-β deposition is a crucial feature of AD, causing neuronal cell death by inducing oxidative damage. Reactive oxygen species (ROS) activate NF-κB, which induces expression of Nucling. Nucling is a pro-apoptotic factor recruiting the apoptosome complex. Lycopene is an antioxidant protecting from oxidative stress-induced c...

2015
Jenny Dworzak Benoît Renvoisé Johnny Habchi Emma V. Yates Christophe Combadière Tuomas P. Knowles Christopher M. Dobson Craig Blackstone Ole Paulsen Philip M. Murphy Koichi M Iijima

Cx3cr1, the receptor for the chemokine Cx3cl1 (fractalkine), has been implicated in the progression and severity of Alzheimer's disease-like pathology in mice, but the underlying mechanisms remain unclear. A complicating factor is that Cx3cr1 has been demonstrated in both neurons and microglia. Here, we have dissected the differences between neuronal and microglial Cx3cr1, specifically by compa...

Journal: :Neurobiology of Aging 2016
K. Abigail Andrews Chris Frost Marc Modat M. Jorge Cardoso Chris C. Rowe Victor Villemagne Nick C. Fox Sebastien Ourselin Jonathan M. Schott

Increased rates of brain atrophy measured from serial magnetic resonance imaging precede symptom onset in Alzheimer's disease and may be useful outcome measures for prodromal clinical trials. Appropriate trial design requires a detailed understanding of the relationships between β-amyloid load and accumulation, and rate of brain change at this stage of the disease. Fifty-two healthy individuals...

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