نتایج جستجو برای: soluble aβ1 42

تعداد نتایج: 198217  

2015
Jung Yeon Lim Charles P. Reighard Damian C. Crowther

Brain-derived neurotrophic factor (BDNF) has a crucial role in learning and memory by promoting neuronal survival and modulating synaptic connectivity. BDNF levels are lower in the brains of individuals with Alzheimer's disease (AD), suggesting a pathogenic involvement. The Drosophila orthologue of BDNF is the highly conserved Neurotrophin 1 (DNT1). BDNF and DNT1 have the same overall protein s...

2017
De-Yu Xia Xin Huang Chong-Feng Bi Lin-Ling Mao Li-Jun Peng Hai-Rong Qian

Alzheimer's disease (AD) is generally defined as the aberrant production of β-amyloid protein (Aβ) and hyperphosphorylated tau protein, which are deposited in β-amyloid plaques (APs) and neurofibrillary tangles (NFTs), respectively. Decreased levels of brain-derived neurotrophic factor (BDNF) have been detected in patients with AD compared to control subjects. However, the underlying molecular ...

2015
Soraya L Valles Diana Aguirre-Rueda Sol Guerra-Ojeda Martin Aldasoro Antonio Iradi Elena Obrador Ma Dolores Mauricio Jose Ma Vila Patricia Marchio

Abstract: Alzheimer ́s disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are ...

Journal: :Journal of Alzheimer's disease : JAD 2014
Michelle Bamji-Mirza Debbie Callaghan Dema Najem Shanshan Shen Mohamed Shaad Hasim Ze Yang Wandong Zhang

One of the hallmarks of Alzheimer's disease (AD) is the accumulation and deposition of amyloid-β (Aβ) peptides in the brain and cerebral vasculature. Aβ evokes neuroinflammation and has been implicated in insulin signaling disruption and JNK-AP1 activation, contributing to AD neuropathologies including oxidative injury and vascular insufficiencies. In this study we aim to better understand the ...

2012
Niklas Mattsson Lawrence Rajendran Henrik Zetterberg Mikael Gustavsson Ulf Andreasson Maria Olsson Gunnar Brinkmalm Johan Lundkvist Laura H. Jacobson Ludovic Perrot Ulf Neumann Herman Borghys Marc Mercken Deborah Dhuyvetter Fredrik Jeppsson Kaj Blennow Erik Portelius

BACE1 is a key enzyme for amyloid-β (Aβ) production, and an attractive therapeutic target in Alzheimer's disease (AD). Here we report that BACE1 inhibitors have distinct effects on neuronal Aβ metabolism, inducing a unique pattern of secreted Aβ peptides, analyzed in cell media from amyloid precursor protein (APP) transfected cells and in cerebrospinal fluid (CSF) from dogs by immunoprecipitati...

2015
Diana Aguirre-Rueda Sol Guerra-Ojeda Martin Aldasoro Antonio Iradi Elena Obrador Maria D. Mauricio Jose Mª Vila Patricia Marchio Soraya L. Valles

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to...

2015
Jianhui Liu Zixuan Liu Yonglan Zhang Fei Yin

BACKGROUND & OBJECTIVES Amyloid β-peptide (Aβ) has been shown to be responsible for senile plaque formation and cell damage in Alzheimer's disease (AD). This study was aimed to explore the role of natural compound icariin on the aggregation and the cytotoxicity of Aβ in vitro. METHODS Thioflavin T (ThT) fluorescence assay and transmission electron microscopy (TEM) imaging were done to determi...

Journal: :Journal of Alzheimer's disease : JAD 2010
Andreas Haldenwanger Paul Eling Andreas Kastrup Helmut Hildebrandt

Decreased delayed recall, decreased amyloid-β peptides (Aβ1-42), and increased tau protein concentration in cerebrospinal fluid (CSF) are generally regarded to be valid neuropsychological and biological markers for Alzheimer's disease (AD). Previous studies failed to demonstrate clear-cut correlations between neuropsychological impairment and CSF markers. In this study we test recent models of ...

2016
Philipp Spitzer Mateja Condic Martin Herrmann Timo Jan Oberstein Marina Scharin-Mehlmann Daniel F. Gilbert Oliver Friedrich Teja Grömer Johannes Kornhuber Roland Lang Juan Manuel Maler

Amyloid-β (Aβ) peptides are the main components of the plaques found in the brains of patients with Alzheimer's disease. However, Aβ peptides are also detectable in secretory compartments and peripheral blood contains a complex mixture of more than 40 different modified and/or N- and C-terminally truncated Aβ peptides. Recently, anti-infective properties of Aβ peptides have been reported. Here,...

Journal: :JAMA neurology 2014
Rahul S Desikan Wesley K Thompson Dominic Holland Christopher P Hess James B Brewer Henrik Zetterberg Kaj Blennow Ole A Andreassen Linda K McEvoy Bradley T Hyman Anders M Dale

IMPORTANCE Converging evidence indicates that clusterin, a chaperone glycoprotein, influences Alzheimer disease neurodegeneration. However, the precise role of clusterin in Alzheimer disease pathogenesis is still not well understood. OBJECTIVE To elucidate the relationship between clusterin, amyloid-β (Aβ), phosphorylated tau (p-tau), and the rate of brain atrophy over time among nondemented ...

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