نتایج جستجو برای: amyloid plaques

تعداد نتایج: 55485  

2017

The identification of amyloid-rich plaques has long been a diagnostic tool for pathologists investigating Alzheimer's disease (AD). The plaques are formed through the accumulation and aggregation of beta-amyloid peptides derived from the amyloid precursor protein (APP; see figure) and are characteristically found in the brain parenchyma and around blood vessels. Although it is clear that APP pl...

Journal: :Neurobiology of aging 2010
Li-Hong Zhang Xin Wang Zhi-Hong Zheng Hao Ren Meredin Stoltenberg Gorm Danscher Liping Huang Ming Rong Zhan-You Wang

Pathological accumulation of beta-amyloid peptide (Abeta) is an early and common feature of Alzheimer's disease (AD). An increased zinc concentration can initiate the deposition of Abeta. The present study aimed to study the expression and distribution patterns of six members of the zinc transporter (ZnT) family, ZnT1, ZnT3, ZnT4, ZnT5, ZnT6, and ZnT7, in the APPswe/PS1dE9 transgenic mouse brai...

Journal: :Neurobiology of aging 2003
T Rees P I Hammond H Soreq S Younkin S Brimijoin

Studies in vitro have suggested that acetylcholinesterase (AChE) may interact with beta-amyloid to promote deposition of amyloid plaques in the brain of patients with Alzheimer's disease. To test that hypothesis in vivo, we crossed Tg2576 mice, which express human amyloid precursor protein and develop plaques at 9 months, with transgenic mice expressing human AChE. The resulting F1 hybrids (FVB...

Journal: :Neurobiology of aging 1996
T L Tekirian G M Cole M J Russell F Yang D R Wekstein E Patel D A Snowdon W R Markesbery J W Geddes

Immunocytochemistry, using antibodies specific for different carboxy termini of beta-amyloid. A beta 40 and A beta 42(43), was used to compare beta-amyloid deposits in aged animal models to nondemented and demented Alzheimer's disease human cases. Aged beagle dogs exhibit diffuse plaques in the absence of neurofibrillary pathology and the aged polar bear brains contain diffuse plaques and PHF-1...

2015
Nina Jährling Klaus Becker Bettina M. Wegenast-Braun Stefan A. Grathwohl Mathias Jucker Hans-Ulrich Dodt Javier Vitorica

Alzheimer´s disease (AD) is the most common neurodegenerative disorder. AD neuropathology is characterized by intracellular neurofibrillary tangles and extracellular β-amyloid deposits in the brain. To elucidate the complexity of AD pathogenesis a variety of transgenic mouse models have been generated. An ideal imaging system for monitoring β-amyloid plaque deposition in the brain of these anim...

2014
Mario M. Dorostkar Steffen Burgold Severin Filser Stefan Barghorn Boris Schmidt Upendra Rao Anumala Heinz Hillen Corinna Klein Jochen Herms

Cognitive decline in Alzheimer's disease is attributed to loss of functional synapses, most likely caused by synaptotoxic, oligomeric forms of amyloid-β. Many treatment options aim at reducing amyloid-β levels in the brain, either by decreasing its production or by increasing its clearance. We quantified the effects of immunotherapy directed against oligomeric amyloid-β in Tg2576 mice, a mouse ...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2010
Samira Kocherhans Amrita Madhusudan Jana Doehner Karin S Breu Roger M Nitsch Jean-Marc Fritschy Irene Knuesel

In addition to the fundamental role of the extracellular glycoprotein Reelin in neuronal development and adult synaptic plasticity, alterations in Reelin-mediated signaling have been suggested to contribute to neuronal dysfunction associated with Alzheimer's disease (AD). In vitro data revealed a biochemical link between Reelin-mediated signaling, Tau phosphorylation, and amyloid precursor prot...

Journal: :Journal of Alzheimer's disease : JAD 2015
Xinhua Zhan Glen C Jickling Bradley P Ander Boryana Stamova DaZhi Liu Patricia F Kao Mariko A Zelin Lee-Way Jin Charles DeCarli Frank R Sharp

The goal of this study was to show that myelin and axons in cortical gray matter are damaged in Alzheimer's disease (AD) brain. Superior temporal gyrus gray matter of AD patients (9 male, 14 female) was compared to cognitively normal controls (8 male, 7 female). Myelin basic protein (MBP) and a degraded myelin basic protein complex (dMBP) were quantified by Western blot. Brain sections were imm...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1990
A M Cataldo R A Nixon

The formation of beta-amyloid in the brains of individuals with Alzheimer disease requires the proteolytic cleavage of a membrane-associated precursor protein. The proteases that may be involved in this process have not yet been identified. Cathepsins are normally intracellular proteolytic enzymes associated with lysosomes; however, when sections from Alzheimer brains were stained by antisera t...

2013
Ester Aso Isidre Ferrer

Senile plaques are mainly composed of different species of fibrillar β-amyloid (Aβ), a product of the cleavage of the β-amyloid precursor protein (APP), and they are surrounded by dystrophic neurites, reactive astrocytes and microglia. Aβ fibrillar deposits also occur in diffuse plaques, subpial deposits and in the wall of the cerebral and meningeal blood vessels in the form of amyloid angiopat...

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