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https://www.readbyqxmd.com/read/29727180/binding-of-cytotoxic-a%C3%AE-25-35-peptide-to-the-dmpc-lipid-bilayer
#1
Amy K Smith, Dmitri K Klimov
Abeta25-35 is a short, cytotoxic, and naturally-occurring fragment of the Alzheimer's Abeta peptide. To map the molecular mechanism of Abeta25-35 binding to the zwitterionic DMPC bilayer, we have performed replica exchange with solute tempering molecular dynamics simulations using all-atom explicit membrane and water models. Consequences of sequence truncation on the binding mechanism have been measured by utilizing as a control our previous simulations probing binding of the longer peptide Abeta10-40 to the same bilayer...
May 4, 2018: Journal of Chemical Information and Modeling
https://www.readbyqxmd.com/read/29673150/immunohistochemical-evidence-from-app-transgenic-mice-for-glutaminyl-cyclase-as-drug-target-to-diminish-pe-abeta-formation
#2
Maike Hartlage-Rübsamen, Alexandra Bluhm, Anke Piechotta, Miriam Linnert, Jens-Ulrich Rahfeld, Hans-Ulrich Demuth, Inge Lues, Peer-Hendrik Kuhn, Stefan F Lichtenthaler, Steffen Roßner, Corinna Höfling
Oligomeric assemblies of neurotoxic amyloid beta (Abeta) peptides generated by proteolytical processing of the amyloid precursor protein (APP) play a key role in the pathogenesis of Alzheimer’s disease (AD). In recent years, a substantial heterogeneity of Abeta peptides with distinct biophysical and cell biological properties has been demonstrated. Among these, a particularly neurotoxic and disease-specific Abeta variant is N-terminally truncated and modified to pyroglutamate (pE-Abeta). Cell biological and animal experimental studies imply the catalysis of this modification by the enzyme glutaminyl cyclase (QC)...
April 17, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/29625180/a%C3%AE-oligomer-uptake-and-the-resulting-inflammatory-response-in-adult-human-astrocytes-are-precluded-by-an-anti-a%C3%AE-single-chain-variable-fragment-in-combination-with-an-apoe-mimetic-peptide
#3
Laia Montoliu-Gaya, Sandra D Mulder, Maaike A C Herrebout, Johannes C Baayen, Sandra Villegas, Robert Veerhuis
An imbalance between production and clearance of soluble amyloid-β (Aβ) initiates the pathological process in sporadic Alzheimer's disease (AD). Aβ-specific antibodies seemed promising as therapeutic option in AD mouse models. In patients, however, vascular side-effects and Aβ-antibody complex-induced microglial and/or perivascular macrophage inflammatory responses were encountered. To prevent inflammatory reactions, we designed a single chain variable fragment (scFv-h3D6), based on monoclonal antibody bapineuzumab (mAb-h3D6), but lacking the Fc region...
June 2018: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/29600401/early-catheter-removal-after-pelvic-floor-reconstructive-surgery-a-randomized-trial
#4
Charelle M Carter-Brooks, Halina M Zyczynski, Pamela A Moalli, Peter G Brodeur, Jonathan P Shepherd
INTRODUCTION AND HYPOTHESIS: Studies have yet to examine the impact of day-of-surgery voiding trials on post-operative urinary retention in women undergoing obliterative and apical suspension procedures for pelvic organ prolapse. Our objective was to evaluate if time to spontaneous void after these procedures is shorter when a voiding trial is performed on the day of surgery compared with our standard practice of post-operative day 1. METHODS: We conducted a randomized, parallel-arm trial in patients undergoing major pelvic floor reconstructive surgery...
March 29, 2018: International Urogynecology Journal
https://www.readbyqxmd.com/read/29561816/synaptic-alterations-in-mouse-models-for-alzheimer-disease-a-special-focus-on-n-truncated-abeta-4-42
#5
Katharina Dietrich, Yvonne Bouter, Michael Müller, Thomas A Bayer
This commentary reviews the role of the Alzheimer amyloid peptide Aβ on basal synaptic transmission, synaptic short-term plasticity, as well as short- and long-term potentiation in transgenic mice, with a special focus on N-terminal truncated Aβ4-42 . Aβ4-42 is highly abundant in the brain of Alzheimer's disease (AD) patients. It demonstrates increased neurotoxicity compared to full length Aβ, suggesting an important role in the pathogenesis of AD. Transgenic Tg4-42 mice, a model for sporadic AD, express human Aβ4-42 in Cornu Ammonis (CA1) neurons, and develop age-dependent hippocampal neuron loss and neurological deficits...
March 21, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/29465978/weaker-n-terminal-interactions-for-the-protective-over-the-causative-a%C3%AE-peptide-dimer-mutants
#6
Bhanushee Sharma, Srivathsan V Ranganathan, Georges Belfort
Knowing that abeta amyloid peptide (Aβ42 ) dimers are the smallest and most abundant neurotoxic oligomers for Alzheimer's disease (AD), we used molecular simulations with advanced sampling methods (replica-exchange) to characterize and compare interactions between the N-termini (residues 1-16) of wild type (WT-WT) and five mutant dimers under constrained and unconstrained conditions. The number of contacts and distances between the N-termini, and contact maps of their conformational landscape illustrate substantial differences for a single residue change...
March 6, 2018: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/29334419/a-metallo-pro-drug-to-target-cu-ii-in-the-context-of-alzheimer-s-disease
#7
Amandine Conte-Daban, Vinita Ambike, Régis Guillot, Nicolas Delsuc, Clotilde Policar, Christelle Hureau
Alzheimer's disease and oxidative stress are connected. In the present communication, we report the use of a MnII -based superoxide dismutase (SOD) mimic ([MnII (L)]+ , 1+ ) as a pro-drug candidate to target CuII -associated events, namely, CuII -induced formation of reactive oxygen species (ROS) and modulation of the amyloid-β (Aβ) peptide aggregation. Complex 1+ is able to remove CuII from Aβ, stop ROS and prevent alteration of Aβ aggregation as would do the corresponding free ligand LH. Using 1+ instead of LH in further biological applications would have the double advantage to avoid the cell toxicity of LH and to benefit from its proved SOD-like activity...
April 6, 2018: Chemistry: a European Journal
https://www.readbyqxmd.com/read/29329646/effects-of-gardenia-jasminoides-extracts-on-cognition-and-innate-immune-response-in-an-adult-drosophila-model-of-alzheimer-s-disease
#8
Wei-Wei Ma, Ye Tao, Yan-Ying Wang, I-Feng Peng
Herbal extracts have been extensively used worldwide for their application on memory improvement, especially among aged and memory-deficit populations. In the present study, the memory loss induced by human Abeta protein over-expression in fruitfly Alzheimer's disease (AD) model was rescued by multiple extracts from Gardenia jasminoides. Three extracts that rich with gardenia yellow, geniposide, and gardenoside components showed distinct rescue effect on memory loss. Further investigation on adding gardenoside into a formula of Ganoderma lucidum, Panax notoginseng and Panax ginseng (GPP) also support its therapeutic effects on memory improvement...
December 2017: Chinese Journal of Natural Medicines
https://www.readbyqxmd.com/read/29260173/fucoidan-inhibits-amyloid-%C3%AE-induced-toxicity-in-transgenic-caenorhabditis-elegans-by-reducing-the-accumulation-of-amyloid-%C3%AE-and-decreasing-the-production-of-reactive-oxygen-species
#9
Xuelian Wang, Kaixuan Yi, Yan Zhao
Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. As the aging population is increasing, AD is becoming one of the leading causes of disability and death among the elderly. However, currently there is no cure for this disease. Fucoidan is a complex sulfated polysaccharide mainly found in brown seaweed. Recent studies have shown that fucoidan is neuroprotective and may have potential to be used for treating and/or preventing neurodegenerative diseases such as AD. In this study, we investigated the effects and possible mechanisms of fucoidan on Abeta induced toxicity in a transgenic Caenorhabditis elegans (C...
January 24, 2018: Food & Function
https://www.readbyqxmd.com/read/29251379/towards-high-throughput-modelling-of-copper-reactivity-induced-by-structural-disorder-in-amyloid-peptides
#10
Giovanni La Penna, Mai Suan Li
Transition metal ions often interact with disordered proteins. The affinity is high enough to compete with structured proteins, but the catalytic activity of the metal centre is often out of control and, therefore, potentially dangerous for cells. An example is a single copper ion interacting with the amyloid-β (Aβ) peptide and triplet dioxygen, an interaction that is fundamental in producing reactive oxygen species in neurodegeneration. High-throughput modelling of the Cu-Aβ-O2 system was performed with the aim of providing a tool to dissect the structural features that characterise dangerous Cu-based catalysts in neurodegeneration...
April 6, 2018: Chemistry: a European Journal
https://www.readbyqxmd.com/read/29209767/neuropathology-of-iatrogenic-creutzfeldt-jakob-disease-and-immunoassay-of-french-cadaver-sourced-growth-hormone-batches-suggest-possible-transmission-of-tauopathy-and-long-incubation-periods-for-the-transmission-of-abeta-pathology
#11
Charles Duyckaerts, Véronique Sazdovitch, Kunie Ando, Danielle Seilhean, Nicolas Privat, Zehra Yilmaz, Laurène Peckeu, Elodie Amar, Emmanuel Comoy, Aleksandra Maceski, Sylvain Lehmann, Jean-Pierre Brion, Jean-Philippe Brandel, Stéphane Haïk
Abeta deposits and tau pathology were investigated in 24 French patients that died from iatrogenic Creutzfeldt-Jakob disease after exposure to cadaver-derived human growth hormone (c-hGH) in the 1980s. Abeta deposits were found only in one case that had experienced one of the longest incubation periods. Three cases had also intracellular tau accumulation. The analysis of 24 batches of c-hGH, produced between 1974 and 1988, demonstrated for the first time the presence of Abeta and tau contaminants in c-hGH (in 17 and 6 batches, respectively)...
February 2018: Acta Neuropathologica
https://www.readbyqxmd.com/read/29151990/robot-embodied-neuronal-networks-as-an-interactive-model-of-learning
#12
Abraham M Shultz, Sangmook Lee, Mary Guaraldi, Thomas B Shea, Holly C Yanco
Background and Objective: The reductionist approach of neuronal cell culture has been useful for analyses of synaptic signaling. Murine cortical neurons in culture spontaneously form an ex vivo network capable of transmitting complex signals, and have been useful for analyses of several fundamental aspects of neuronal development hitherto difficult to clarify in situ . However, these networks lack the ability to receive and respond to sensory input from the environment as do neurons in vivo ...
2017: Open Neurology Journal
https://www.readbyqxmd.com/read/29130469/-heparan-sulphates-amyloidosis-and-neurodegeneration
#13
REVIEW
C Vera, J A Alvarez-Orozco, A Maiza, S Chantepie, R N Chehin, M O Ouidja, D Papy-Garcia
INTRODUCTION: A number of neurodegenerative disorders have been linked directly to the accumulation of amyloid fibres. These fibres are made up of proteins or peptides with altered structures and which join together in vivo in association with heparan sulphate-type polysaccharides. AIMS: To examine the most recent concepts in the biology of heparan sulphates and their role in the aggregation of the peptide Abeta, of tau protein, of alpha-synuclein and of prions...
November 16, 2017: Revista de Neurologia
https://www.readbyqxmd.com/read/29094781/cognitive-impairment-in-glucocerebrosidase-gba-associated-pd-not-primarily-associated-with-cerebrospinal-fluid-abeta-and-tau-profiles
#14
Stefanie Lerche, Claudia Schulte, Karin Srulijes, Andrea Pilotto, Tim W Rattay, Ann-Kathrin Hauser, Elke Stransky, Christian Deuschle, Ilona Csoti, Ingolf Lachmann, Henrik Zetterberg, Inga Liepelt-Scarfone, Thomas Gasser, Walter Maetzler, Daniela Berg, Kathrin Brockmann
BACKGROUND: A proportion of idiopathic Parkinson's disease patients (PDidiopathic ) with dementia show altered CSF profiles of amyloid β (Aβ) and Tau. PD patients with Glucocerebrosidase (GBA) mutations (PDGBA ) present with even more cognitive decline than seen in PDidiopathic . OBJECTIVE: The objective of this study was to evaluate whether CSF profiles of Aβ and tau are associated with the prominent cognitive impairment in PDGBA . METHODS: CSF levels of Aβ1-42 , t-Tau, p-Tau, and total alpha-synuclein were assessed in 479 participants (50 PDGBA , 308 PDidiopathic , 121 healthy controls)...
December 2017: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29048250/inhibition-of-abeta-proteotoxicity-by-paeoniflorin-in-caenorhabditis-elegans-through-regulation-of-oxidative-and-heat-shock-stress-responses
#15
Liping Ai, Fan Yang, Jie Song, Yan Chen, Lingyun Xiao, Qiangqiang Wang, Liangyi Wang, Haifeng Li, Tao Lei, Zebo Huang
Alzheimer's disease (AD) is a common form of dementia and amyloid-β peptide (Aβ) aggregation is considered to be one of its main causes. Paeoniflorin has been previously shown to attenuate cognitive damage inflicted by exogenous Aβ protein. Using transgenic Caenorhabditis elegans models expressing human Aβ1-42 , we demonstrate here that paeoniflorin can delay progressive paralysis caused by endogenous Aβ expression and reduce the amount of toxic Aβ oligomers in vivo, although it has no effect on Aβ aggregation in vitro...
December 14, 2017: Rejuvenation Research
https://www.readbyqxmd.com/read/28927263/molecular-and-cellular-basis-of-neurodegeneration-in-alzheimer-s-disease
#16
REVIEW
Sangyun Jeong
The most common form of senile dementia is Alzheimer's disease (AD), which is characterized by the extracellular deposition of amyloid β-peptide (Aβ) plaques and the intracellular formation of neurofibrillary tangles (NFTs) in the cerebral cortex. Tau abnormalities are commonly observed in many neurodegenerative diseases including AD, Parkinson's disease, and Pick's disease. Interestingly, tau-mediated formation of NFTs in AD brains shows better correlation with cognitive impairment than Aβ plaque accumulation; pathological tau alone is sufficient to elicit frontotemporal dementia, but it does not cause AD...
September 30, 2017: Molecules and Cells
https://www.readbyqxmd.com/read/28910085/cholesterol-changes-the-mechanisms-of-a%C3%AE-peptide-binding-to-the-dmpc-bilayer
#17
Christopher Lockhart, Dmitri K Klimov
Using isobaric-isothermal all-atom replica-exchange molecular dynamics (REMD) simulations, we investigated the equilibrium binding of Aβ10-40 monomers to the zwitterionic dimyristoylphosphatidylcholine (DMPC) bilayer containing cholesterol. Our previous REMD simulations, which studied binding of the same peptide to the cholesterol-free DMPC bilayer, served as a control, against which we measured the impact of cholesterol. Our findings are as follows. First, addition of cholesterol to the DMPC bilayer partially expels the Aβ peptide from the hydrophobic core and promotes its binding to bilayer polar headgroups...
October 23, 2017: Journal of Chemical Information and Modeling
https://www.readbyqxmd.com/read/28882310/studying-tau-protein-propagation-and-pathology-in-the-mouse-brain-using-adeno-associated-viruses
#18
Susanne Wegmann, Rachel E Bennett, Ana S Amaral, Bradley T Hyman
The progressive spread of pathological brain lesions containing aggregated tau protein is a hallmark of Alzheimer's disease and other neurodegenerative diseases. In AD, this process follows a distinct pattern along neuronal connections from the entorhinal cortex to hippocampal areas and further on through the limbic system. In other tauopathies, the spread of tau appears less hierarchical throughout the brain, and also nonpathological tau is reported to cross-synaptic connections in the brain. To be able to study the process of cell-to-cell transport of tau and the associated neurotoxicity in the brain in vivo, adeno-associated virus-mediated expression of tau can be used to express different forms of tau in distinct brain areas in rodent models...
2017: Methods in Cell Biology
https://www.readbyqxmd.com/read/28691712/erratum-reduction-of-abeta-amyloid-pathology-in-appps1-transgenic-mice-in-the-absence-of-gut-microbiota
#19
T Harach, N Marungruang, N Duthilleul, V Cheatham, K D Mc Coy, G Frisoni, J J Neher, F Fåk, M Jucker, T Lasser, T Bolmont
This corrects the article DOI: 10.1038/srep41802.
July 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28625940/prodromal-stage-of-disease-dementia-with-lewy-bodies-how-to-diagnose-in-practice
#20
REVIEW
Frédéric Blanc, Marc Verny
Disease with Lewy bodies or dementia with Lewy bodies (DLB), particularly at the prodromal stage, is a complex disease to diagnose because of different clinical beginnings and variable paths in terms of clinical expression. Thus DLB can be entcountered in different input modes: mild cognitive impairment, depression, acute behavioral disorders, confusion and delirium, or sleep disorders. In the aim to better diagnose the disease, should be sought obviously to search for the key symptoms: fluctuations, hallucinations, extra-pyramidal syndrome, and REM sleep behavior disorder...
June 1, 2017: Gériatrie et Psychologie Neuropsychiatrie du Vieillissement
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