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Aggregation of deposits animal model

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https://www.readbyqxmd.com/read/28424619/retinal-and-circulating-mirnas-in-age-related-macular-degeneration-an-in-vivo-animal-and-human-study
#1
Giovanni L Romano, Chiara B M Platania, Filippo Drago, Salvatore Salomone, Marco Ragusa, Cristina Barbagallo, Cinzia Di Pietro, Michele Purrello, Michele Reibaldi, Teresio Avitabile, Antonio Longo, Claudio Bucolo
Age related macular degeneration (AMD) is the leading cause of blindness among people aged 50 and over. Retinal deposition of amyloid-β (Aβ) aggregates in AMD patients has suggested a potential link between AMD and Alzheimer's disease (AD). We have evaluated the differential retinal expression profile of miRNAs in a rat model of AMD elicited by Aβ. A serum profile of miRNAs in AMD patients has been also assessed using single TaqMan assay. Analysis of retina from rats intravitreally injected with Aβ revealed that miR-27a, miR-146a, and miR-155 were up-regulated in comparison to control rats...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28293166/protein-remodeling-factors-as-potential-therapeutics-for-neurodegenerative-disease
#2
REVIEW
Meredith E Jackrel, James Shorter
Protein misfolding is implicated in numerous neurodegenerative disorders including amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease, and Huntington's disease. A unifying feature of patients with these disorders is the accumulation of deposits comprised of misfolded protein. Aberrant protein folding can cause toxicity through a loss or gain of protein function, or both. An intriguing therapeutic approach to counter these disorders is the application of protein-remodeling factors to resolve these misfolded conformers and return the proteins to their native fold and function...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28218748/hiv-tat-protein-and-amyloid-%C3%AE-peptide-form-multifibrillar-structures-that-cause-neurotoxicity
#3
Alina Hategan, Mario A Bianchet, Joseph Steiner, Elena Karnaukhova, Eliezer Masliah, Adam Fields, Myoung-Hwa Lee, Alex M Dickens, Norman Haughey, Emilios K Dimitriadis, Avindra Nath
Deposition of amyloid-β plaques is increased in the brains of HIV-infected individuals, and the HIV transactivator of transcription (Tat) protein affects amyloidogenesis through several indirect mechanisms. Here, we investigated direct interactions between Tat and amyloid-β peptide. Our in vitro studies showed that in the presence of Tat, uniform amyloid fibrils become double twisted fibrils and further form populations of thick unstructured filaments and aggregates. Specifically, Tat binding to the exterior surfaces of the Aβ fibrils increases β-sheet formation and lateral aggregation into thick multifibrillar structures, thus producing fibers with increased rigidity and mechanical resistance...
April 2017: Nature Structural & Molecular Biology
https://www.readbyqxmd.com/read/28109886/truncated-prion-protein-prp226-a-structural-view-on-its-role-in-amyloid-disease
#4
Valerija Kovač, Blaž Zupančič, Gregor Ilc, Janez Plavec, Vladka Čurin Šerbec
In the brain of patients with transmissible spongiform encephalopathies, besides PrP(Sc) aggregates, deposition of truncated PrP molecules was described. Jansen et al. reported two clinical cases with deposition of C-terminally truncated PrP, one of them ending with Tyr226. We have previously described the discovery of monoclonal antibody V5B2 that selectively recognizes this version of the prion protein, which we called PrP226*. Using monoclonal antibody V5B2 we showed that accumulation of PrP226* is characteristic for most types of human and animal TSEs...
January 19, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28044060/molecular-interaction-between-type-2-diabetes-and-alzheimer-s-disease-through-cross-seeding-of-protein-misfolding
#5
I Moreno-Gonzalez, G Edwards Iii, N Salvadores, M Shahnawaz, R Diaz-Espinoza, C Soto
Numerous epidemiological studies have shown a significantly higher risk for development of Alzheimer's disease (AD) in patients affected by type 2 diabetes (T2D), but the molecular mechanism responsible for this association is presently unknown. Both diseases are considered protein misfolding disorders associated with the accumulation of protein aggregates; amyloid-beta (Aβ) and tau in the brain during AD, and islet amyloid polypeptide (IAPP) in pancreatic islets in T2D. Formation and accumulation of these proteins follows a seeding-nucleation model, where a misfolded aggregate or 'seed' promotes the rapid misfolding and aggregation of the native protein...
January 3, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/27958227/establishment-of-a-novel-mouse-model-of-coronary-microembolization
#6
Yuan-Yuan Cao, Zhang-Wei Chen, Jian-Guo Jia, Ao Chen, You Zhou, Yong Ye, Yan-Hua Gao, Yan Xia, Shu-Fu Chang, Jian-Ying Ma, Ju-Ying Qian, Jun-Bo Ge
BACKGROUND: Coronary microembolization (CME) has been frequently seen in acute coronary syndromes and percutaneous coronary intervention. Small animal models are required for further studies of CME related to severe prognosis. This study aimed to explore a new mouse model of CME. METHODS: The mouse model of CME was established by injecting polystyrene microspheres into the left ventricular chamber during 15-s occlusion of the ascending aorta. Based on the average diameter and dosage used, 30 C57BL/6 male mice were randomly divided into five groups (n = 6 in each): 9 μm/500,000, 9 μm/800,000, 17 μm/200,000, 17 μm/500,000, and sham groups...
December 20, 2016: Chinese Medical Journal
https://www.readbyqxmd.com/read/27936457/genetic-disruption-of-nrf2-promotes-the-development-of-necroinflammation-and-liver-fibrosis-in-a-mouse-model-of-hfe-hereditary-hemochromatosis
#7
Tiago L Duarte, Carolina Caldas, Ana G Santos, Sandro Silva-Gomes, Andreia Santos-Gonçalves, Maria João Martins, Graça Porto, José Manuel Lopes
BACKGROUND AND AIMS: In hereditary hemochromatosis, iron deposition in the liver parenchyma may lead to fibrosis, cirrhosis and hepatocellular carcinoma. Most cases are ascribed to a common mutation in the HFE gene, but the extent of clinical expression is greatly influenced by the combined action of yet unidentified genetic and/or environmental modifying factors. In mice, transcription factor NRF2 is a critical determinant of hepatocyte viability during exposure to acute dietary iron overload...
April 2017: Redox Biology
https://www.readbyqxmd.com/read/27896391/histological-aspects-of-the-fixed-particle-model-of-stone-formation-animal-studies
#8
REVIEW
Saeed R Khan
Crystallization by itself is not harmful as long as the crystals are not retained in the kidneys and are allowed to pass freely down the renal tubules to be excreted in the urine. A number of theories have been proposed, and studies performed, to determine the mechanisms involved in crystal retention within the kidneys. It has been suggested that urinary transit through the nephron is too fast for crystals to grow large enough to be retained. Thus, free particle mechanism alone cannot lead to stone formation, and there must be a mechanism for crystal fixation within the kidneys...
February 2017: Urolithiasis
https://www.readbyqxmd.com/read/27829314/bone-morphogenetic-protein-2-but-not-mesenchymal-stromal-cells-exert-regenerative-effects-on-canine-and-human-nucleus-pulposus-cells
#9
Frances C Bach, Alberto Miranda-Bedate, Ferdi W M van Heel, Frank M Riemers, Margot C M E Müller, Laura B Creemers, Keita Ito, Karin Benz, Björn P Meij, Marianna A Tryfonidou
Chronic back pain is related to intervertebral disc (IVD) degeneration and dogs are employed as animal models to develop growth factor- and cell-based regenerative treatments. In this respect, the differential effects of transforming growth factor beta-1 (TGF-β1) and bone morphogenetic protein-2 (BMP2) on canine and human chondrocyte-like cells (CLCs) derived from the nucleus pulposus of degenerated IVDs were studied. Human and canine CLCs were cultured in 3D microaggregates in basal culture medium supplemented with/without TGF-β1 (10 ng/mL) or BMP2 (100 or 250 ng/mL)...
March 2017: Tissue Engineering. Part A
https://www.readbyqxmd.com/read/27751744/the-alzheimer-s-related-amyloid-beta-peptide-is-internalised-by-r28-neuroretinal-cells-and-disrupts-the-microtubule-associated-protein-2-map-2
#10
George Taylor-Walker, Savannah A Lynn, Eloise Keeling, Rosie Munday, David A Johnston, Anton Page, Jennifer A Scott, Srini Goverdhan, Andrew J Lotery, J Arjuna Ratnayaka
Age-related Macular Degeneration (AMD) is a common, irreversible blinding condition that leads to the loss of central vision. AMD has a complex aetiology with both genetic as well as environmental risks factors, and share many similarities with Alzheimer's disease. Recent findings have contributed significantly to unravelling its genetic architecture that is yet to be matched by molecular insights. Studies are made more challenging by observations that aged and AMD retinas accumulate the highly pathogenic Alzheimer's-related Amyloid beta (Aβ) group of peptides, for which there appears to be no clear genetic basis...
December 2016: Experimental Eye Research
https://www.readbyqxmd.com/read/27585306/neurodegeneration-in-an-animal-model-of-chronic-amyloid-beta-oligomer-infusion-is-counteracted-by-antibody-treatment-infused-with-osmotic-pumps
#11
Ahmadali Sajadi, Chloé Provost, Brendon Pham, Jonathan Brouillette
Decline in hippocampal-dependent explicit memory (memory for facts and events) is one of the earliest clinical symptom of Alzheimer's disease (AD). It is well established that synapse loss and ensuing neurodegeneration are the best predictors for memory impairments in AD. Latest studies have emphasized the neurotoxic role of soluble amyloid-beta oligomers (Aβo) that begin to accumulate in the human brain approximately 10 to 15 yr before the clinical symptoms become apparent. Many reports indicate that soluble Aβo correlate with memory deficits in AD models and humans...
August 14, 2016: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/27363697/immunotherapy-targeting-pyroglutamate-3-a%C3%AE-prospects-and-challenges
#12
REVIEW
Holger Cynis, Jeffrey L Frost, Helen Crehan, Cynthia A Lemere
Immunization against amyloid-β (Aβ) peptides deposited in Alzheimer's disease (AD) has shown considerable therapeutic effect in animal models however, the translation into human Alzheimer's patients is challenging. In recent years, a number of promising Aβ immunotherapy trials failed to reach primary study endpoints. Aside from uncertainties in the selection of patients and the start and duration of treatment, these results also suggest that the mechanisms underlying AD are still not fully understood. Thorough characterizations of protein aggregates in AD brain have revealed a conspicuous heterogeneity of Aβ peptides enabling the study of the toxic potential of each of the major forms...
2016: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/27293325/prions-prion-like-prionoids-and-neurodegenerative-disorders
#13
REVIEW
Ashok Verma
Prion diseases or transmissible spongiform encephalopathies are fatal neurodegenerative diseases characterized by the aggregation and deposition of the misfolded prion protein in the brain. α-synuclein (α-syn)-associated multiple system atrophy has been recently shown to be caused by a bona fide α-syn prion strain. Several other misfolded native proteins such as β-amyloid, tau and TDP-43 share some aspects of prions although none of them is shown to be transmissible in nature or in experimental animals...
April 2016: Annals of Indian Academy of Neurology
https://www.readbyqxmd.com/read/27188290/rhizophora-mucronata-attenuates-beta-amyloid-induced-cognitive-dysfunction-oxidative-stress-and-cholinergic-deficit-in-alzheimer-s-disease-animal-model
#14
Natarajan Suganthy, Dicson Sheeja Malar, Kasi Pandima Devi
Alzheimer's disease (AD) is a progressive neurodegenerative disorder, characterized by accumulation and deposition of Aβ peptide in human brain. The present study aimed to determine the protective effect of catechin rich extract of MERM (methanolic extract of Rhizophora mucronata) on Aβ (25-35) induced cognitive impairment and neuronal toxicity in mice. In the present study AD characteristics were induced by intracerberoventricular administration of aggregated Aβ (25-35) in the Swiss albino mice. Learning and memory deficits were assessed using behavioral assays such as Morris water maze, Y-maze and step down avoidance tasks...
August 2016: Metabolic Brain Disease
https://www.readbyqxmd.com/read/27070146/humanized-tau-mice-with-regionalized-amyloid-exhibit-behavioral-deficits-but-no-pathological-interaction
#15
Michael J Yetman, Stephanie W Fowler, Joanna L Jankowsky
Alzheimer's disease (AD) researchers have struggled for decades to draw a causal link between extracellular Aβ aggregation and intraneuronal accumulation of microtubule-associated protein tau. The amyloid cascade hypothesis posits that Aβ deposition promotes tau hyperphosphorylation, tangle formation, cell loss, vascular damage, and dementia. While the genetics of familial AD and the pathological staging of sporadic disease support this sequence of events, attempts to examine the molecular mechanism in transgenic animal models have largely relied on models of other inherited tauopathies as the basis for testing the interaction with Aβ...
2016: PloS One
https://www.readbyqxmd.com/read/26933687/an-anticancer-drug-suppresses-the-primary-nucleation-reaction-that-initiates-the-production-of-the-toxic-a%C3%AE-42-aggregates-linked-with-alzheimer-s-disease
#16
Johnny Habchi, Paolo Arosio, Michele Perni, Ana Rita Costa, Maho Yagi-Utsumi, Priyanka Joshi, Sean Chia, Samuel I A Cohen, Martin B D Müller, Sara Linse, Ellen A A Nollen, Christopher M Dobson, Tuomas P J Knowles, Michele Vendruscolo
The conversion of the β-amyloid (Aβ) peptide into pathogenic aggregates is linked to the onset and progression of Alzheimer's disease. Although this observation has prompted an extensive search for therapeutic agents to modulate the concentration of Aβ or inhibit its aggregation, all clinical trials with these objectives have so far failed, at least in part because of a lack of understanding of the molecular mechanisms underlying the process of aggregation and its inhibition. To address this problem, we describe a chemical kinetics approach for rational drug discovery, in which the effects of small molecules on the rates of specific microscopic steps in the self-assembly of Aβ42, the most aggregation-prone variant of Aβ, are analyzed quantitatively...
February 2016: Science Advances
https://www.readbyqxmd.com/read/26912432/small-animal-pet-imaging-of-tau-pathology-with-18f-thk5117-in-2-transgenic-mouse-models
#17
Matthias Brendel, Anna Jaworska, Federico Probst, Felix Overhoff, Viktoria Korzhova, Simon Lindner, Janette Carlsen, Peter Bartenstein, Ryuichi Harada, Yukitsuka Kudo, Christian Haass, Fred Van Leuven, Nobuyuki Okamura, Jochen Herms, Axel Rominger
Abnormal accumulation of tau aggregates in the brain is one of the hallmarks of Alzheimer disease neuropathology. We visualized tau deposition in vivo with the previously developed 2-arylquinoline derivative (18)F-THK5117 using small-animal PET in conjunction with autoradiography and immunohistochemistry gold standard assessment in 2 transgenic mouse models expressing hyperphosphorylated tau. Small-animal PET recordings were obtained in groups of P301S (n = 11) and biGT mice (n = 16) of different ages, with age-matched wild-type (WT) serving as controls...
May 2016: Journal of Nuclear Medicine: Official Publication, Society of Nuclear Medicine
https://www.readbyqxmd.com/read/26780369/sequential-extraction-of-soluble-and-insoluble-alpha-synuclein-from-parkinsonian-brains
#18
Rina Bandopadhyay
Alpha-synuclein (α-syn) protein is abundantly expressed mainly within neurons, and exists in a number of different forms - monomers, tetramers, oligomers and fibrils. During disease, α-syn undergoes conformational changes to form oligomers and high molecular weight aggregates that tend to make the protein more insoluble. Abnormally aggregated α-syn is a neuropathological feature of Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Biochemical characterization and analysis of insoluble α-syn using buffers with increasing detergent strength and high-speed ultracentrifugation provides a powerful tool to determine the development of α-syn pathology associated with disease progression...
January 5, 2016: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/26758850/attenuation-of-%C3%AE-amyloid-deposition-and-neurotoxicity-by-chemogenetic-modulation-of-neural-activity
#19
Peng Yuan, Jaime Grutzendler
UNLABELLED: Aberrant neural hyperactivity has been observed in early stages of Alzheimer's disease (AD) and may be a driving force in the progression of amyloid pathology. Evidence for this includes the findings that neural activity may modulate β-amyloid (Aβ) peptide secretion and experimental stimulation of neural activity can increase amyloid deposition. However, whether long-term attenuation of neural activity prevents the buildup of amyloid plaques and associated neural pathologies remains unknown...
January 13, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/26758828/altered-intrinsic-pyramidal-neuron-properties-and-pathway-specific-synaptic-dysfunction-underlie-aberrant-hippocampal-network-function-in-a-mouse-model-of-tauopathy
#20
Clair A Booth, Jonathan Witton, Jakub Nowacki, Krasimira Tsaneva-Atanasova, Matthew W Jones, Andrew D Randall, Jonathan T Brown
UNLABELLED: The formation and deposition of tau protein aggregates is proposed to contribute to cognitive impairments in dementia by disrupting neuronal function in brain regions, including the hippocampus. We used a battery of in vivo and in vitro electrophysiological recordings in the rTg4510 transgenic mouse model, which overexpresses a mutant form of human tau protein, to investigate the effects of tau pathology on hippocampal neuronal function in area CA1 of 7- to 8-month-old mice, an age point at which rTg4510 animals exhibit advanced tau pathology and progressive neurodegeneration...
January 13, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
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