نتایج جستجو برای: amyloid plaques

تعداد نتایج: 55485  

Journal: :Drug metabolism reviews 2014
Elizabeth Drolle Francis Hane Brenda Lee Zoya Leonenko

Alzheimer's disease (AD) is a devastating neurodegenerative disease characterized by dementia and memory loss for which no cure or effective prevention is currently available. Neurodegeneration in AD is linked to formation of amyloid plaques found in brain tissues of Alzheimer's patients during post-mortem examination. Amyloid plaques are composed of amyloid fibrils and small oligomers - insolu...

Journal: :Journal of Alzheimer's disease : JAD 2013
Rob J A Nabuurs Remco Natté Fenna M de Ronde Ingrid Hegeman-Kleinn Jouke Dijkstra Sjoerd G van Duinen Andrew G Webb Annemieke J Rozemuller Mark A van Buchem Louise van der Weerd

Cerebral deposits of amyloid-β peptides (Aβ) form the neuropathological hallmarks of Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA). In the brain, Aβ can aggregate as insoluble fibrils present in amyloid plaques and vascular amyloid, or as diffuse plaques consisting of mainly non-fibrillar Aβ. Previously, magnetic resonance imaging (MRI) has been shown to be capable of detecting...

Journal: :Journal of neuropathology and experimental neurology 2010
Henri J Huttunen Daniel Havas Camilla Peach Cory Barren Stephan Duller Weiming Xia Matthew P Frosch Birgit Hutter-Paier Manfred Windisch Dora M Kovacs

Cerebral accumulation of amyloid-beta (Abeta) is characteristic of Alzheimer disease and of amyloid precursor protein (APP) transgenic mice. Here, we assessed the efficacy of CI-1011, an inhibitor of acyl-coenzyme A:cholesterol acyltransferase, which is suitable for clinical use, in reducing amyloid pathology in both young (6.5 months old) and aged (16 months old) human APP transgenic mice. Tre...

Journal: :Brain 2009
John A. Ronald Yuanxin Chen Lisa Bernas Hagen H. Kitzler Kem A. Rogers Robert A. Hegele Brian K. Rutt

Two significant barriers have limited the development of effective treatment of Alzheimer's disease. First, for many cases the aetiology is unknown and likely multi-factorial. Among these factors, hypercholesterolemia is a known risk predictor and has been linked to the formation of beta-amyloid plaques, a pathological hallmark this disease. Second, standardized diagnostic tools are unable to d...

2013
Youssef Zaim Wadghiri Jialin Li Jinhuan Wang Dung Minh Hoang Yanjie Sun Hong Xu Wai Tsui Yongsheng Li Allal Boutajangout Andrew Wang Mony de Leon Thomas Wisniewski

Amyloid plaques are a key pathological hallmark of Alzheimer's disease (AD). The detection of amyloid plaques in the brain is important for the diagnosis of AD, as well as for following potential amyloid targeting therapeutic interventions. Our group has developed several contrast agents to detect amyloid plaques in vivo using magnetic resonance microimaging (µMRI) in AD transgenic mice, where ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2017
Jay Rasmussen Jasmin Mahler Natalie Beschorner Stephan A Kaeser Lisa M Häsler Frank Baumann Sofie Nyström Erik Portelius Kaj Blennow Tammaryn Lashley Nick C Fox Diego Sepulveda-Falla Markus Glatzel Adrian L Oblak Bernardino Ghetti K Peter R Nilsson Per Hammarström Matthias Staufenbiel Lary C Walker Mathias Jucker

The molecular architecture of amyloids formed in vivo can be interrogated using luminescent conjugated oligothiophenes (LCOs), a unique class of amyloid dyes. When bound to amyloid, LCOs yield fluorescence emission spectra that reflect the 3D structure of the protein aggregates. Given that synthetic amyloid-β peptide (Aβ) has been shown to adopt distinct structural conformations with different ...

2011
Hisako Muramatsu1 Katsunori Yokoi Lan Chen Keiko Ichihara-Tanaka Terutoshi Kimura Takashi Muramatsu

BACKGROUND Midkine is a heparin-binding cytokine involved in cell survival and various inflammatory processes. Midkine accumulates in senile plaques of patients with Alzheimer's disease, while it counteracts the cytotoxic effects of amyloid β-peptide and inhibits its oligomerization. The present study was conducted to understand the role of midkine upon plaque formation of amyloid β-peptide. ...

Journal: :Journal of neuropathology and experimental neurology 2013
Alberto Serrano-Pozo Alona Muzikansky Teresa Gómez-Isla John H Growdon Rebecca A Betensky Matthew P Frosch Bradley T Hyman

Although it is clear that astrocytes and microglia cluster around dense-core amyloid plaques in Alzheimer disease (AD), whether they are primarily attracted to amyloid deposits or are just reacting to plaque-associated neuritic damage remains elusive. We postulate that astrocytes and microglia may differentially respond to fibrillar amyloid β. Therefore, we quantified the size distribution of d...

Journal: :International Journal of Biological Sciences 2008
Kun Zou Tomoji Maeda Makoto Michikawa Hiroto Komano

Melanie Meyer-Luehmann et al. recently reported that amyloid plaques form extremely rapidly-within one day, in three mouse models of Alzheimer’s disease studied longitudinally in vivo [1]. However, the ‘rapid appearance’ of ‘newborn’ amyloid plaques can also be the result of delayed visualization of existing amyloid plaques, which is caused by the increase in the concentration of methoxy-XO4, a...

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