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Aggregation of deposits animal model

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https://www.readbyqxmd.com/read/29117254/link-n-the-missing-link-towards-intervertebral-disc-repair-is-species-specific
#1
Frances C Bach, Lisanne T Laagland, Michael P Grant, Laura B Creemers, Keita Ito, Björn P Meij, Fackson Mwale, Marianna A Tryfonidou
INTRODUCTION: Degeneration of the intervertebral disc (IVD) is a frequent cause for back pain in humans and dogs. Link-N stabilizes proteoglycan aggregates in cartilaginous tissues and exerts growth factor-like effects. The human variant of Link-N facilitates IVD regeneration in several species in vitro by inducing Smad1 signaling, but it is not clear whether this is species specific. Dogs with IVD disease could possibly benefit from Link-N treatment, but Link-N has not been tested on canine IVD cells...
2017: PloS One
https://www.readbyqxmd.com/read/29027056/curcumin-affords-neuroprotection-and-inhibits-%C3%AE-synuclein-aggregation-in-lipopolysaccharide-induced-parkinson-s-disease-model
#2
Neha Sharma, Bimla Nehru
Parkinson's disease (PD) pathology is characterized by the abnormal accumulation and aggregation of the pre-synaptic protein α-synuclein in the dopaminergic neurons as Lewy bodies (LBs). Curcumin, which plays a neuroprotective role in various animal models of PD, was found to directly modulate the aggregation of α-synuclein in in vitro as well as in in vivo studies. While curcumin has been shown to exhibit strong anti-oxidant and anti-inflammatory properties, there are a number of other possible mechanisms by which curcumin may alter α-synuclein aggregation which still remains obscure...
October 12, 2017: Inflammopharmacology
https://www.readbyqxmd.com/read/28993573/measurement-of-nanoparticle-exposure-in-crematoriums-and-estimation-of-respiratory-deposition-of-the-nanoparticles-by-number-and-size-distribution
#3
Nobuhuki Kato, Yasuto Mastui, Masaki Takaoka, Minoru Yoneda
OBJECTIVES: Nanoparticles (NPs), including hazardous substances, are generated in crematoriums due to the high temperatures during the combustion process. NPs are reported to greatly impact animals' health by reaching the alveoli and being carried to the entire body through the blood stream. However, studies in crematoriums have yet to assess workers' exposure to the generated NPs. The purpose of this study is to assess workers' exposure to NPs released in crematoriums. METHODS: Field surveys were conducted in three crematoriums with an emphasis on cremation, bone rearrangement and cleaning processes...
October 7, 2017: Journal of Occupational Health
https://www.readbyqxmd.com/read/28917837/memantine-inhibits-%C3%AE-amyloid-aggregation-and-disassembles-preformed-%C3%AE-amyloid-aggregates
#4
Kaori Takahashi-Ito, Mitsuhiro Makino, Keiko Okado, Taisuke Tomita
Memantine, an uncompetitive glutamatergic N-methyl-d-aspartate (NMDA) receptor antagonist, is widely used as a medication for the treatment of Alzheimer's disease (AD). We previously reported that chronic treatment of AD with memantine reduces the amount of insoluble β-amyloid (Aβ) and soluble Aβ oligomers in animal models of AD. The mechanisms by which memantine reduces Aβ levels in the brain were evaluated by determining the effect of memantine on Aβ aggregation using thioflavin T and transmission electron microscopy...
November 4, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28894090/seed-induced-acceleration-of-amyloid-%C3%AE-mediated-neurotoxicity-in-vivo
#5
Ramona F Sowade, Thomas R Jahn
Seeded propagation of amyloid-beta (Aβ) pathology is suggested to contribute to the progression of Alzheimer's disease. Local overproduction of aggregation-prone Aβ variants could explain the focal initiation of a seeding cascade that subsequently triggers widespread pathology. Several animal models support this seeding concept by demonstrating accelerated Aβ deposition following inoculation with Aβ-containing homogenates, however its role in progressive neurodegeneration remains unclear. Here, we present a non-invasive approach to study Aβ seeding processes in vivo using Drosophila models...
September 11, 2017: Nature Communications
https://www.readbyqxmd.com/read/28862836/generation-of-clickable-pittsburgh-compound-b-for-the-detection-and-capture-of-%C3%AE-amyloid-in-alzheimer-s-disease-brain
#6
Ian Diner, Jeromy Dooyema, Marla Gearing, Lary C Walker, Nicholas T Seyfried
The benzothiazole-aniline derivative Pittsburgh Compound B (PiB) is the prototypical amyloid affinity probe developed for the in vivo positron emission tomography (PET) detection of amyloid beta (Aβ) deposits in Alzheimer's disease (AD). Specific high-affinity binding sites for PiB have been found to vary among AD cases with comparable Aβ load, and they are virtually absent on human-sequence Aβ deposits in animal models, none of which develop the full phenotype of AD. PiB thus could be an informative probe for studying the pathobiology of Aβ, but little is known about the localization of PiB binding at the molecular or structural level...
October 18, 2017: Bioconjugate Chemistry
https://www.readbyqxmd.com/read/28662102/a-novel-monoclonal-antibody-against-the-n-terminus-of-a%C3%AE-1-42-reduces-plaques-and-improves-cognition-in-a-mouse-model-of-alzheimer-s-disease
#7
Hai-Yan Xing, Bin Li, Dan Peng, Chun-Yan Wang, Guan-Ying Wang, Pan Li, Ying-Ying Le, Ji-Ming Wang, George Ye, Jian-Hong Chen
Senile plaques consisting of Amyloid-beta (Aβ) peptides, in particular Aβ1-42, are the hallmark of Alzheimer's disease (AD) and have been the primary therapeutic targets. Passive immunotherapy with monoclonal antibodies (mAbs) has shown initial success in mouse models of AD. However, the existing Aβ-directed mAbs mostly were tested on animal models or patients with advanced disease. The effects and mechanisms of mAbs on animals or human trial participants in the prodromal phase of AD are not fully clarified...
2017: PloS One
https://www.readbyqxmd.com/read/28526436/intracranial-il-17a-overexpression-decreases-cerebral-amyloid-angiopathy-by-upregulation-of-abca1-in-an-animal-model-of-alzheimer-s-disease
#8
Junling Yang, Jinghong Kou, Robert Lalonde, Ken-Ichiro Fukuchi
Neuroinflammation is a pervasive feature of Alzheimer's disease (AD) and characterized by activated microglia, increased proinflammatory cytokines and/or infiltrating immune cells. T helper 17 (Th17) cells are found in AD brain parenchyma and interleukin-17A (IL-17A) is identified around deposits of aggregated amyloid β protein (Aβ). However, the role of IL-17A in AD pathogenesis remains elusive. We overexpressed IL-17A in an AD mouse model via recombinant adeno-associated virus serotype 5 (rAAV5)-mediated intracranial gene delivery...
October 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28433262/primary-motor-cortex-alterations-in-alzheimer-disease-a-study-in-the-3xtg-ad-model
#9
E Orta-Salazar, A I Feria-Velasco, S Díaz-Cintra
INTRODUCTION: In humans and animal models, Alzheimer disease (AD) is characterised by accumulation of amyloid-β peptide (Aβ) and hyperphosphorylated tau protein, neuronal degeneration, and astrocytic gliosis, especially in vulnerable brain regions (hippocampus and cortex). These alterations are associated with cognitive impairment (loss of memory) and non-cognitive impairment (motor impairment). The purpose of this study was to identify cell changes (neurons and glial cells) and aggregation of Aβ and hyperphosphorylated tau protein in the primary motor cortex (M1) in 3xTg-AD mouse models at an intermediate stage of AD...
April 19, 2017: Neurología: Publicación Oficial de la Sociedad Española de Neurología
https://www.readbyqxmd.com/read/28424619/retinal-and-circulating-mirnas-in-age-related-macular-degeneration-an-in-vivo-animal-and-human-study
#10
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
#11
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
#12
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
#13
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...
February 26, 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
#14
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...
September 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/27958227/establishment-of-a-novel-mouse-model-of-coronary-microembolization
#15
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
#16
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
#17
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
#18
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
#19
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
#20
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
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