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https://www.readbyqxmd.com/read/28636676/mitochondrion-to-endoplasmic-reticulum-apposition-length-in-zebrafish-embryo-spinal-progenitors-is-unchanged-in-response-to-perturbations-associated-with-alzheimer-s-disease
#1
Morgan Newman, Lena Halter, Anne Lim, Michael Lardelli
Mutations in the human genes PRESENILIN1 (PSEN1), PRESENILIN2 (PSEN2) and AMYLOID BETA A4 PRECURSOR PROTEIN (APP) have been identified in familial Alzheimer's disease (AD). The length of mitochondrion-endoplasmic reticulum (M-ER) appositions is increased in Psen1-/-/Psen2-/- double knockout murine embryonic fibroblasts and in fibroblasts from AD-affected individuals. Development of an easily accessible, genetically manipulable, in vivo system for studying M-ER appositions would be valuable so we attempted to manipulate M-ER apposition length in zebrafish (Danio rerio) embryos...
2017: PloS One
https://www.readbyqxmd.com/read/28634550/sortilin-related-receptor-expression-in-human-neural-stem-cells-derived-from-alzheimer-s-disease-patients-carrying-the-apoe-epsilon-4-allele
#2
Alen Zollo, Zoe Allen, Helle F Rasmussen, Filomena Iannuzzi, Yichen Shi, Agnete Larsen, Thorsten J Maier, Carmela Matrone
Alzheimer's disease (AD) is the most common form of dementia in the elderly; important risk factors are old age and inheritance of the apolipoprotein E4 (APOE4) allele. Changes in amyloid precursor protein (APP) binding, trafficking, and sorting may be important AD causative factors. Secretase-mediated APP cleavage produces neurotoxic amyloid-beta (Aβ) peptides, which form lethal deposits in the brain. In vivo and in vitro studies have implicated sortilin-related receptor (SORL1) as an important factor in APP trafficking and processing...
2017: Neural Plasticity
https://www.readbyqxmd.com/read/28631483/amyloid-beta-peptide-folding-in-reverse-micelles
#3
Gozde Eskici, Paul H Axelsen
Previously published experimental studies have suggested that when the 40-residue amyloid beta peptide is encapsulated in a reverse micelle, it folds into a structure that may nucleate amyloid fibril formation (Yeung and Axelsen, J. Am. Chem. Soc. 134:6061, 2012). The factors that induce the formation of this structure have now been identified in a multi-microsecond simulation of the same reverse micelle system that was studied experimentally. Key features of the polypeptide-micelle interaction include the anchoring of a hydrophobic residue cluster into the reverse micelle surface, the formation of a beta turn at the anchor point that brings N- and C-terminal segments of the polypeptide into proximity, high ionic strength that promotes intramolecular hydrogen bond formation, and deformation of the reverse micelle surface to facilitate interactions with the surface along the entire length of the polypeptide...
June 20, 2017: Journal of the American Chemical Society
https://www.readbyqxmd.com/read/28626017/amyloid-beta-peptide-is-needed-for-cgmp-induced-long-term-potentiation-and-memory
#4
Agostino Palmeri, Roberta Ricciarelli, Walter Gulisano, Daniela Rivera, Claudia Rebosio, Elisa Calcagno, Maria Rosaria Tropea, Silvia Conti, Utpal Das, Subhojit Roy, Maria A Pronzato, Ottavio Arancio, Ernesto Fedele, Daniela Puzzo
High levels of amyloid-beta peptide (Aβ) have been related to Alzheimer's disease pathogenesis. However, in the healthy brain, low physiologically relevant concentrations of Aβ are necessary for long-term potentiation (LTP) and memory. Because cGMP plays a key role in these processes, here we investigated whether the cyclic nucleotide cGMP influences Aβ levels and function during LTP and memory. We demonstrate that the increase of cGMP levels by the phosphodiesterase-5 inhibitors (PDE5-Is) sildenafil and vardenafil induces a parallel release of Aβ due to a change in the approximation of amyloid precursor protein (APP) and the β-site APP cleaving enzyme 1 (BACE1)...
June 16, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28626014/bace1-cleavage-site-selection-critical-for-amyloidogenesis-and-alzheimer-s-pathogenesis
#5
Shuting Zhang, Zhe Wang, Fang Cai, Mingming Zhang, Yili Wu, Jing Zhang, Weihong Song
Mutations in amyloid β precursor protein (APP) gene alter APP processing, either causing familial Alzheimer's Disease (AD) or protecting against dementia. Under normal conditions beta-site APP cleaving enzyme 1 (BACE1) cleaves APP at minor Asp(1) site to generate C99 for amyloid β protein (Aβ) production, and predominantly at major Glu(11) site to generate C89, resulting in truncated Aβ production. We discovered that A673V mutation, the only recessive AD-associated APP mutation, shifted the preferential β-cleavage site of BACE1 in APP from the Glu(11) site to the Asp(1) site both in male and female transgenic mice in vivo and in cell lines and primary neuronal culture derived from timed pregnant rats in vitro, resulting in a much higher C99 level and C99/C89 ratio...
June 16, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28624356/vascular-ageing-underlying-mechanisms-and-clinical-implications
#6
REVIEW
Ageliki Laina, Konstantinos Stellos, Kimon Stamatelopoulos
Epidemiological studies have shown that ageing is a major non-reversible risk factor for cardiovascular disease. Vascular ageing starts early in life and is characterized by a gradual change of vascular structure and function resulting in increased arterial stiffening. At the present review we discuss the role of the most important molecular pathways involved in vascular ageing, their association with arterial stiffening and possible novel therapeutic targets that may delay this otherwise irreversible degenerating process...
June 14, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28622510/microbial-genetic-composition-tunes-host-longevity
#7
Bing Han, Priya Sivaramakrishnan, Chih-Chun J Lin, Isaiah A A Neve, Jingquan He, Li Wei Rachel Tay, Jessica N Sowa, Antons Sizovs, Guangwei Du, Jin Wang, Christophe Herman, Meng C Wang
Homeostasis of the gut microbiota critically influences host health and aging. Developing genetically engineered probiotics holds great promise as a new therapeutic paradigm to promote healthy aging. Here, through screening 3,983 Escherichia coli mutants, we discovered that 29 bacterial genes, when deleted, increase longevity in the host Caenorhabditis elegans. A dozen of these bacterial mutants also protect the host from age-related progression of tumor growth and amyloid-beta accumulation. Mechanistically, we discovered that five bacterial mutants promote longevity through increased secretion of the polysaccharide colanic acid (CA), which regulates mitochondrial dynamics and unfolded protein response (UPR(mt)) in the host...
June 15, 2017: Cell
https://www.readbyqxmd.com/read/28621364/single-molecule-probing-of-amyloid-nano-ensembles-using-the-polymer-nanoarray-approach
#8
Sibaprasad Maity, Ekaterina Viazovkina, Alexander Gall, Yuri L Lyubchenko
Soluble amyloid-beta (Aβ) oligomers are the prime causative agents of cognitive deficits during early stages of Alzheimer's disease (AD). The transient nature of the oligomers makes them difficult to characterize by traditional techniques, suggesting that advanced approaches are necessary. Previously developed fluorescence-based tethered approach for probing intermolecular interactions (TAPIN) and AFM-based single-molecule force spectroscopy are capable of probing dimers of Aβ peptides. In this paper, a novel polymer nanoarray approach to probe trimers and tetramers formed by the Aβ(14-23) segment of Aβ protein at the single-molecule level is applied...
June 16, 2017: Physical Chemistry Chemical Physics: PCCP
https://www.readbyqxmd.com/read/28619586/determination-of-acidity-constants-and-prediction-of-electrophoretic-separation-of-amyloid-beta-peptides
#9
Roger Peró-Gascón, Fernando Benavente, José Barbosa, Victoria Sanz-Nebot
In this paper we describe a strategy to estimate by CE the acidity constants (pKa) of complex polyprotic peptides from their building peptide fragments. CE has been used for the determination of the pKas of five short polyprotic peptides that cover all the sequence of amyloid beta (Aβ) peptides 1-40 and 1-42 (Aβ fragments 1-15, 10-20, 20-29, 25-35 and 33-42). First, the electrophoretic mobility (me) was measured as a function of pH of the background electrolyte (BGE) in the pH range 2-12 (bare fused silica capillary, I=25mM and T=25°C)...
June 3, 2017: Journal of Chromatography. A
https://www.readbyqxmd.com/read/28617071/an-endothelial-link-between-the-benefits-of-physical-exercise-in-dementia
#10
Lianne J Trigiani, Edith Hamel
The current absence of a disease-modifying treatment for Alzheimer's disease (AD) and vascular cognitive impairment and dementia (VCID) highlights the necessity for investigating the benefits of non-pharmacological approaches such as physical exercise (PE). Although evidence exists to support an association between regular PE and higher scores on cognitive function tests, and a slower rate of cognitive decline, there is no clear consensus on the underlying molecular mechanisms of the advantages of PE. This review seeks to summarize the positive effects of PE in human and animal studies while highlighting the vascular link between these benefits...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28611935/gastrointestinal-amyloidosis-review-of-the-literature
#11
REVIEW
Kyle Rowe, Jon Pankow, Fredy Nehme, William Salyers
Gastrointestinal amyloidosis (GIA), a protein deposition disorder, represents a complex common pathway that encompasses multiple etiologies and presentations. It represents a significant diagnostic and treatment challenge. The disease results from the deposition of insoluble extracellular protein fragments that have been rendered resistant to digestion. GIA can be acquired or genetic, and most commonly results from chronic inflammatory disorders (AA amyloidosis), hematologic malignancy (AL amyloidosis), and end-stage renal disease (Beta-2 amyloidosis)...
May 8, 2017: Curēus
https://www.readbyqxmd.com/read/28611418/arrestins-contribute-to-amyloid-beta-induced-cell-death-via-modulation-of-autophagy-and-the-%C3%AE-7nach-receptor-in-sh-sy5y-cells
#12
Yi-Qing Liu, Meng-Qi Jia, Zhao-Hong Xie, Xiao-Fei Liu, Hui-Yang, Xiao-Lei Zheng, Hui-Qing Yuan, Jian-Zhong Bi
Amyloid β-protein (Aβ) is believed to contribute to the development of Alzheimer's disease (AD). Here we showed that Aβ25-35 rapidly caused activation of autophagy, subsequently leading to reduction of autophagy associated with cellular apoptosis. Further investigation revealed that the accumulation of β-arrestin 1 (ARRB1) caused by Aβ25-35 contributed to the induction of autophagic flux. The depletion of ARRB1 led to decreases in the expression of LC3B, Atg7, and Beclin-1, which are essential for the initiation of autophagy...
June 13, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28607171/astrocyte-transforming-growth-factor-beta-1-protects-synapses-against-a%C3%AE-oligomers-in-alzheimer-s-disease-model
#13
Luan Pereira Diniz, Vanessa Tortelli, Isadora Matias, Juliana Morgado, Ana Paula Bérgamo Araujo, Helen M Melo, Gisele S Seixas da Silva, Soniza V Alves-Leon, Jorge M de Souza, Sergio T Ferreira, Fernanda G De Felice, Flávia Carvalho Alcantara Gomes
Alzheimer's disease (AD) is characterized by progressive cognitive decline, increasingly attributed to neuronal dysfunction induced by amyloid-β oligomers (AβOs). Although the impact of AβOs on neurons has been extensively studied, only recently have the possible effects of AβOs on astrocytes begun to be investigated. Given the key roles of astrocytes in synapse formation, plasticity and function, we sought to investigate the impact of AβOs on astrocytes, and to determine if this impact is related to the deleterious actions of AβOs on synapses...
June 12, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28604235/discovery-validation-and-optimization-of-cerebrospinal-fluid-biomarkers-for-use-in-parkinson-s-disease
#14
Lucia Farotti, Silvia Paciotti, Anna Tasegian, Paolo Eusebi, Lucilla Parnetti
Parkinson's disease (PD) is a complex and phenotypically heterogeneous neurodegenerative disease, for which the diagnosis is mainly based on clinical parameters (even if neuroimaging plays a role in diagnostic assessment); as a consequence, misdiagnosis is common, especially in early stages. Thus, there is an urgent need of having available biomarkers in order to achieve an early and accurate diagnosis. Since molecular changes in the brain are reliably and timely reflected in cerebrospinal fluid (CSF), CSF represents an ideal source for biomarkers of different pathophysiological processes characterizing the disease since its early phases...
June 19, 2017: Expert Review of Molecular Diagnostics
https://www.readbyqxmd.com/read/28601278/laquinimod-has-no-effects-on-brain-volume-or-cellular-cns-composition-in-the-f1-3xtg-ad-c3h-mouse-model-of-alzheimer-s-disease
#15
Rehana Z Hussain, William A Miller-Little, Doris Lambracht-Washington, Tom C Jaramillo, Masaya Takahashi, Shanrong Zhang, Min Fu, Gary R Cutter, Liat Hayardeny, Craig M Powell, Roger N Rosenberg, Olaf Stüve
BACKGROUND: Laquinimod is an anti-inflammatory agent with good central nervous system (CNS) bioavailability, and neuroprotective and myelorestorative properties. A clinical trial in patients with multiple sclerosis demonstrated that laquinimod significantly reduced loss of brain volume. The cellular substrate or molecular events underlying that treatment effect are unknown. In this study, we aimed to explore laquinimod's potential effects on brain volume, animal behavior, cellular numbers and composition of CNS-intrinsic cells and mononuclear cells within the CNS, amyloid beta (Aβ) accumulation and tau phosphorylation in the F1 3xTg-AD/C3H mouse model of Alzheimer's disease...
August 15, 2017: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/28599849/the-amyloid-beta-precursor-protein-the-unappreciated-cerebral-anticoagulant
#16
EDITORIAL
Alvin H Schmaier
No abstract text is available yet for this article.
June 2, 2017: Thrombosis Research
https://www.readbyqxmd.com/read/28595629/identification-and-description-of-three-families-with-familial-alzheimer-disease-that-segregate-variants-in-the-sorl1-gene
#17
Håkan Thonberg, Huei-Hsin Chiang, Lena Lilius, Charlotte Forsell, Anna-Karin Lindström, Charlotte Johansson, Jenny Björkström, Steinunn Thordardottir, Kristel Sleegers, Christine Van Broeckhoven, Annica Rönnbäck, Caroline Graff
Alzheimer disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia. The majority of AD cases are sporadic, while up to 5% are families with an early onset AD (EOAD). Mutations in one of the three genes: amyloid beta precursor protein (APP), presenilin 1 (PSEN1) or presenilin 2 (PSEN2) can be disease causing. However, most EOAD families do not carry mutations in any of these three genes, and candidate genes, such as the sortilin-related receptor 1 (SORL1), have been suggested to be potentially causative...
June 9, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28593141/glycosyl-chains-and-25-hydroxycholesterol-contribute-to-the-intracellular-transport-of-amyloid-beta-a%C3%AE-42-in-jurkat-t-cells
#18
Neha Sharma, KeangOK Baek, Huong T T Phan, Naofumi Shimokawa, Masahiro Takagi
Amyloid beta (Aβ) is a peptide responsible for the development of Alzheimer's disease (AD). Misfolding and accumulation of endogenous Aβ can lead to neural cell apoptosis through endoplasmic reticulum (ER) stress. Added exogenous Aβ can also result in ER stress, leading to neurotoxicity and apoptosis, which is identical to that caused by the endogenous peptide. We have speculated that the endocytic transport of Aβ causes ER stress and have previously shown that the oxysterol, in particular, 7-ketocholesterol (7-keto) induces more surface interaction between Aβ-42 and Jurkat cells than cholesterol...
June 2017: FEBS Open Bio
https://www.readbyqxmd.com/read/28593105/photobiomodulation-with-near-infrared-light-helmet-in-a-pilot-placebo-controlled-clinical-trial-in-dementia-patients-testing-memory-and-cognition
#19
Marvin H Berman, James P Halper, Trent W Nichols, H Jarrett, Alan Lundy, Jason H Huang
Alzheimer's disease (AD) is a common, chronic expensive debilitating neurodegenerative disease with no current treatments to prevent the physical deterioration of the brain and the consequent cognitive deficits. The current pathophysiology of Alzheimer's disease is the accumulation of neurofibrillary tangles (NFTs) of hyperphosphorylated tau protein and amyloid-beta (Aβ) plaques. Antibody therapy of Tau and Amyloid beta, vaccines and other methods to decrease Tau and or Amyloid have not been successful after considerable pharmaceutical and biotech efforts...
2017: Journal of neurology and neuroscience
https://www.readbyqxmd.com/read/28592401/transgenic-tomatoes-expressing-the-6f-peptide-and-ezetimibe-prevent-diet-induced-increases-of-interferon-%C3%AE-and-cholesterol-25-hydroxylase-in-jejunum
#20
Pallavi Mukherjee, Greg Hough, Arnab Chattopadhyay, Mohamad Navab, Hannah R Fogelman, David Meriwether, Kevin Williams, Steven Bensinger, Travis Moller, Kym F Faull, Aldons J Lusis, Luisa Iruela-Arispe, Kristina I Bostrom, Peter Tontonoz, Srinivasa T Reddy, Alan M Fogelman
Feeding LDLR-null mice a Western diet (WD) increased the expression of interferon beta (IFN-β) in jejunum as determined by RT-qPCR, immunohistochemistry (IHC), and by ELISA (all p <0.0001). WD also increased the expression of cholesterol 25-hydroxylase (CH25H) as measured by RT-qPCR (p <0.0001), IHC (p = 0.0019), and ELISA (p <0.0001) resulting in increased levels of 25-hydroxycholesterol (25-OHC) in jejunum as determined by LC-MS/MS (p <0.0001). Adding Ezetimibe at 10 mg/kg/day or adding a concentrate of transgenic tomatoes expressing the 6F peptide (Tg6F) at 0...
June 7, 2017: Journal of Lipid Research
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