نتایج جستجو برای: amyloid deposition

تعداد نتایج: 126596  

2010
Dorene M Rentz Joseph J Locascio John A Becker Erin K Moran Elisha Eng Randy L Buckner Reisa A Sperling Keith A Johnson

OBJECTIVE To determine whether amyloid deposition is associated with impaired neuropsychological (NP) performance and whether cognitive reserve (CR) modifies this association. METHODS In 66 normal elderly controls and 17 patients with Alzheimer disease (AD), we related brain retention of Pittsburgh Compound B (PiB) to NP performance and evaluated the impact of CR using education and American ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2005
Jin-Ping Li Martha L Escobar Galvis Feng Gong Xiao Zhang Eyal Zcharia Shula Metzger Israel Vlodavsky Robert Kisilevsky Ulf Lindahl

Amyloid diseases encompass >20 medical disorders that include amyloid protein A (AA) amyloidosis, Alzheimer's disease, and type 2 diabetes. A common feature of these conditions is the selective organ deposition of disease-specific fibrillar proteins, along with the sulfated glycosaminoglycan, heparan sulfate. We have generated transgenic mice that overexpress human heparanase and have tested th...

2018
Dosuke Iwadate Eiko Hasegawa Junichi Hoshino Noriko Hayami Keiichi Sumida Masayuki Yamanouchi Akinari Sekine Masahiro Kawada Rikako Hiramatsu Tatsuya Suwabe Naoki Sawa Mitsuhiro Yuasa Atsushi Wake Takeshi Fujii Kenichi Ohashi Kenmei Takaichi Yoshifumi Ubara

A 55-year-old man was admitted to our institute to undergo evaluation for proteinuria (5.4 g/day) with lambda-type Bence-Jones protein (BJP). Primary amyloid light chain (AL) amyloidosis and acquired factor X deficiency were diagnosed. High-dose melphalan combined with autologous stem cell transplantation was performed. After three years, the patient's proteinuria normalized, he was negative fo...

2017
Johannes Steffen Markus Krohn Christina Schwitlick Thomas Brüning Kristin Paarmann Claus U. Pietrzik Henrik Biverstål Baiba Jansone Oliver Langer Jens Pahnke

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer's disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ an...

Journal: :Indian Journal of Pathology and Microbiology 2020

Journal: :Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 1975

Journal: :Alzheimer Disease & Associated Disorders 2014

2014
Macdonald I.R DeBay D.R Reid G.A O’Leary T.P Jollymore C.T Mawko G Burrell S Martin E Bowen C.V Brown R.E Darvesh S

Brain glucose hypometabolism has been observed in Alzheimer's disease (AD) patients, and is detected with (18)F radiolabelled glucose, using positron emission tomography. A pathological hallmark of AD is deposition of brain β- amyloid plaques that may influence cerebral glucose metabolism. The five times familial AD (5XFAD) mouse is a model of brain amyloidosis exhibiting AD-like phenotypes. Th...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2012
Adam W Bero Adam Q Bauer Floy R Stewart Brian R White John R Cirrito Marcus E Raichle Joseph P Culver David M Holtzman

Brain region-specific deposition of extracellular amyloid plaques principally composed of aggregated amyloid-β (Aβ) peptide is a pathological signature of Alzheimer's disease (AD). Recent human neuroimaging data suggest that resting-state functional connectivity strength is reduced in patients with AD, cognitively normal elderly harboring elevated amyloid burden, and in advanced aging. Interest...

Journal: :Neuron 2009
Reisa A. Sperling Peter S. LaViolette Kelly O'Keefe Jacqueline O'Brien Dorene M. Rentz Maija Pihlajamaki Gad Marshall Bradley T. Hyman Dennis J. Selkoe Trey Hedden Randy L. Buckner J. Alex Becker Keith A. Johnson

Alzheimer's disease (AD) has been associated with functional alterations in a distributed network of brain regions linked to memory function, with a recent focus on the cortical regions collectively known as the default network. Posterior components of the default network, including the precuneus and posterior cingulate, are particularly vulnerable to early deposition of amyloid beta-protein, o...

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