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Tau oligomers

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https://www.readbyqxmd.com/read/28426964/ipsc-derived-human-microglia-like-cells-to-study-neurological-diseases
#1
Edsel M Abud, Ricardo N Ramirez, Eric S Martinez, Luke M Healy, Cecilia H H Nguyen, Sean A Newman, Andriy V Yeromin, Vanessa M Scarfone, Samuel E Marsh, Cristhian Fimbres, Chad A Caraway, Gianna M Fote, Abdullah M Madany, Anshu Agrawal, Rakez Kayed, Karen H Gylys, Michael D Cahalan, Brian J Cummings, Jack P Antel, Ali Mortazavi, Monica J Carson, Wayne W Poon, Mathew Blurton-Jones
Microglia play critical roles in brain development, homeostasis, and neurological disorders. Here, we report that human microglial-like cells (iMGLs) can be differentiated from iPSCs to study their function in neurological diseases, like Alzheimer's disease (AD). We find that iMGLs develop in vitro similarly to microglia in vivo, and whole-transcriptome analysis demonstrates that they are highly similar to cultured adult and fetal human microglia. Functional assessment of iMGLs reveals that they secrete cytokines in response to inflammatory stimuli, migrate and undergo calcium transients, and robustly phagocytose CNS substrates...
April 19, 2017: Neuron
https://www.readbyqxmd.com/read/28421539/%C3%AE-synuclein-aggregates-with-%C3%AE-amyloid-or-tau-in-human-red-blood-cells-correlation-with-antioxidant-capability-and-physical-exercise-in-human-healthy-subjects
#2
Simona Daniele, Deborah Pietrobono, Jonathan Fusi, Caterina Iofrida, Lucia Chico, Lucia Petrozzi, Annalisa Lo Gerfo, Filippo Baldacci, Fabio Galetta, Gabriele Siciliano, Ubaldo Bonuccelli, Gino Santoro, Maria Letizia Trincavelli, Ferdinando Franzoni, Claudia Martini
Neurodegenerative disorders (NDs) are characterized by abnormal accumulation/misfolding of specific proteins, primarily α-synuclein (α-syn), β-amyloid1-42 (Aβ), and tau, in both brain and peripheral tissue. In addition to homo-oligomers, the role of α-syn interactions with Aβ or tau has gradually emerged. The altered protein accumulation has been related to both oxidative stress and physical activity; nevertheless, no correlation among the presence of peripheral α-syn hetero-aggregates, antioxidant capacity, and physical exercise has been discovered as of yet...
April 18, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28420982/tau-oligomers-cytotoxicity-propagation-and-mitochondrial-damage
#3
REVIEW
Scott S Shafiei, Marcos J Guerrero-Muñoz, Diana L Castillo-Carranza
Aging has long been considered as the main risk factor for several neurodegenerative disorders including a large group of diseases known as tauopathies. Even though neurofibrillary tangles (NFTs) have been examined as the main histopathological hallmark, they do not seem to play a role as the toxic entities leading to disease. Recent studies suggest that an intermediate form of tau, prior to NFT formation, the tau oligomer, is the true toxic species. However, the mechanisms by which tau oligomers trigger neurodegeneration remain unknown...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28420443/tau-phosphorylation-induced-by-severe-closed-head-traumatic-brain-injury-is-linked-to-the-cellular-prion-protein
#4
Richard Rubenstein, Binggong Chang, Natalia Grinkina, Eleanor Drummond, Peter Davies, Meir Ruditzky, Deep Sharma, Kevin Wang, Thomas Wisniewski
Studies in vivo and in vitro have suggested that the mechanism underlying Alzheimer's disease (AD) neuropathogenesis is initiated by an interaction between the cellular prion protein (PrP(C)) and amyloid-β oligomers (Aβo). This PrP(C)-Aβo complex activates Fyn kinase which, in turn, hyperphosphorylates tau (P-Tau) resulting in synaptic dysfunction, neuronal loss and cognitive deficits. AD transgenic mice lacking PrP(C) accumulate Aβ, but show normal survival and no loss of spatial learning and memory suggesting that PrP(C) functions downstream of Aβo production but upstream of intracellular toxicity within neurons...
April 18, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28392295/oleocanthal-ameliorates-amyloid-%C3%AE-oligomers-toxicity-on-astrocytes-and-neuronal-cells-in-vitro-studies
#5
Yazan S Batarseh, Loqman A Mohamed, Sweilem B Al Rihani, Youssef M Mousa, Abu Bakar Siddique, Khalid A El Sayed, Amal Kaddoumi
Extra-virgin olive oil (EVOO) has several health promoting effects. Evidence have shown that EVOO attenuates the pathology of amyloid-β (Aβ) and improves cognitive function in experimental animal models, suggesting it's potential to protect and reduce the risk of developing Alzheimer's disease (AD). Available studies have linked this beneficial effect to oleocanthal, one of the active components in EVOO. The effect of oleocanthal against AD pathology has been linked to its ability to attenuate Aβ and tau aggregation in vitro, and enhance Aβ clearance from the brains of wild-type and AD transgenic mice in vivo...
April 7, 2017: Neuroscience
https://www.readbyqxmd.com/read/28382304/tau-oligomers-in-cerebrospinal-fluid-in-alzheimer-s-disease
#6
Urmi Sengupta, Erik Portelius, Oskar Hansson, Kathleen Farmer, Diana Castillo-Carranza, Randall Woltjer, Henrik Zetterberg, Douglas Galasko, Kaj Blennow, Rakez Kayed
OBJECTIVE: With an increasing incidence of Alzheimer's disease (AD) and neurodegenerative tauopathies, there is an urgent need to develop reliable biomarkers for the diagnosis and monitoring of the disease, such as the recently discovered toxic tau oligomers. Here, we aimed to demonstrate the presence of tau oligomers in the cerebrospinal fluid (CSF) of patients with cognitive deficits, and to determine whether tau oligomers could serve as a potential biomarker for AD. METHODS: A multicentric collaborative study involving a double-blinded analysis with a total of 98 subjects with moderate to severe AD (N = 41), mild AD (N = 31), and nondemented control subjects (N = 26), and two pilot studies of 33 total patients with AD (N = 19) and control (N = 14) subjects were performed...
April 2017: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/28377712/pgc-1%C3%AE-or-fndc5-is-involved-in-modulating-the-effects-of-a%C3%AE-1-42-oligomers-on-suppressing-the-expression-of-bdnf-a-beneficial-factor-for-inhibiting-neuronal-apoptosis-a%C3%AE-deposition-and-cognitive-decline-of-app-ps1-tg-mice
#7
De-Yu Xia, Xin Huang, Chong-Feng Bi, Lin-Ling Mao, Li-Jun Peng, Hai-Rong Qian
Alzheimer's disease (AD) is generally defined as the aberrant production of β-amyloid protein (Aβ) and hyperphosphorylated tau protein, which are deposited in β-amyloid plaques (APs) and neurofibrillary tangles (NFTs), respectively. Decreased levels of brain-derived neurotrophic factor (BDNF) have been detected in patients with AD compared to control subjects. However, the underlying molecular mechanisms driving the downregulation of the BDNF remain unknown. Therefore, we explored the mechanisms underlying the regulation of BDNF in the neurons of APP/PS1 transgenic (Tg) mice, an AD experimental model...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28356893/alzheimer-s-toxic-amyloid-beta-oligomers-unwelcome-visitors-to-the-na-k-atpase-alpha3-docking-station
#8
Thomas DiChiara, Nadia DiNunno, Jeffrey Clark, Riana Lo Bu, Erika N Cline, Madeline G Rollins, Yuesong Gong, David L Brody, Stephen G Sligar, Pauline T Velasco, Kirsten L Viola, William L Klein
Toxic amyloid beta oligomers (AβOs) are known to accumulate in Alzheimer's disease (AD) and in animal models of AD. Their structure is heterogeneous, and they are found in both intracellular and extracellular milieu. When given to CNS cultures or injected ICV into non-human primates and other non-transgenic animals, AβOs have been found to cause impaired synaptic plasticity, loss of memory function, tau hyperphosphorylation and tangle formation, synapse elimination, oxidative and ER stress, inflammatory microglial activation, and selective nerve cell death...
March 2017: Yale Journal of Biology and Medicine
https://www.readbyqxmd.com/read/28352227/a-novel-genetic-screen-identifies-modifiers-of-age-dependent-amyloid-%C3%AE-toxicity-in-the-drosophila-brain
#9
Lautaro F Belfiori-Carrasco, María S Marcora, Nadia I Bocai, M Fernanda Ceriani, Laura Morelli, Eduardo M Castaño
The accumulation of amyloid β peptide (Aβ) in the brain of Alzheimer's disease (AD) patients begins many years before clinical onset. Such process has been proposed to be pathogenic through the toxicity of Aβ soluble oligomers leading to synaptic dysfunction, phospho-tau aggregation and neuronal loss. Yet, a massive accumulation of Aβ can be found in approximately 30% of aged individuals with preserved cognitive function. Therefore, within the frame of the "amyloid hypothesis", compensatory mechanisms and/or additional neurotoxic or protective factors need to be considered and investigated...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28348546/dementia-with-lewy-bodies-molecular-pathology-in-the-frontal-cortex-in-typical-and-rapidly-progressive-forms
#10
Paula Garcia-Esparcia, Irene López-González, Oriol Grau-Rivera, María Francisca García-Garrido, Anusha Konetti, Franc Llorens, Saima Zafar, Margarita Carmona, José Antonio Del Rio, Inga Zerr, Ellen Gelpi, Isidro Ferrer
OBJECTIVES: The goal of this study was to assess mitochondrial function, energy, and purine metabolism, protein synthesis machinery from the nucleolus to the ribosome, inflammation, and expression of newly identified ectopic olfactory receptors (ORs) and taste receptors (TASRs) in the frontal cortex of typical cases of dementia with Lewy bodies (DLB) and cases with rapid clinical course (rpDLB: 2 years or less) compared with middle-aged non-affected individuals, in order to learn about the biochemical abnormalities underlying Lewy body pathology...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28155596/inhibition-of-tau-protein-aggregation-by-rhodanine-based-compounds-solubilized-via-specific-formulation-additives-to-improve-bioavailability-and-cell-viability
#11
Marcus Pickhardt, Carmen Lawatscheck, Hans G Börner, Eckhard Mandelkow
BACKGROUND: Anti-aggregation drugs play an important role in therapeutic approaches for Alzheimer's disease. We have previously developed a number of compounds that are able to inhibit the pathological aggregation of Tau protein. One common obstacle to application is the limited penetration across the plasma membranes into cells, where Tau aggregation occurs in the cytosol. We used an inducible N2a cell line which expresses the repeat domain of tau and develops tau aggregates. OBJECTIVE: Several peptide-polymer conjugates were synthesized to enhance the uptake of compounds into cells and thus to improve their biomedical application...
February 1, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28147245/angiotensin-1-7-administration-attenuates-alzheimer-s-disease-like-neuropathology-in-rats-with-streptozotocin-induced-diabetes-via-mas-receptor-activation
#12
Jin-Liang Chen, Dong-Ling Zhang, Yue Sun, Yu-Xing Zhao, Ke-Xiang Zhao, Die Pu, Qian Xiao
Diabetes mellitus (DM) is associated with cognitive deficits and an increased risk of Alzheimer's disease (AD). Recently, a newly identified heptapeptide of the renin-angiotensin system (RAS), angiotensin-(1-7) [Ang-(1-7)], was found to protect against brain damage. This study investigated the effects of Ang-(1-7) on diabetes-induced cognitive deficits. Sprague-Dawley rats were randomly divided into four groups. Diabetes was induced via single i.p. streptozotocin (STZ) injections. Ten weeks after diabetes induction, rats in each group received an intracerebral-ventricular (ICV) infusion of either vehicle, Ang-(1-7) alone, or Ang-(1-7)+A779 daily for two weeks...
January 29, 2017: Neuroscience
https://www.readbyqxmd.com/read/28137266/the-neurotoxicity-of-amyloid-%C3%AE-protein-oligomers-is-reversible-in-a-primary-neuron-model
#13
Daisuke Tanokashira, Naomi Mamada, Fumiko Yamamoto, Kaori Taniguchi, Akira Tamaoka, Madepalli K Lakshmana, Wataru Araki
Alzheimer's disease (AD) is characterized by the accumulation of extracellular amyloid β-protein (Aβ) and intracellular hyperphosphorylated tau proteins. Recent evidence suggests that soluble Aβ oligomers elicit neurotoxicity and synaptotoxicity, including tau abnormalities, and play an initiating role in the development of AD pathology. In this study, we focused on the unclarified issue of whether the neurotoxicity of Aβ oligomers is a reversible process. Using a primary neuron culture model, we examined whether the neurotoxic effects induced by 2-day treatment with Aβ42 oligomers (Aβ-O) are reversible during a subsequent 2-day withdrawal period...
January 31, 2017: Molecular Brain
https://www.readbyqxmd.com/read/28088900/synaptic-plasticity-dementia-and-alzheimer-disease
#14
Stephen D Skaper, Laura Facci, Morena Zusso, Pietro Giusti
Neuroplasticity is not only shaped by learning and memory but is also a mediator of responses to neuron attrition and injury (compensatory plasticity). As an ongoing process it reacts to neuronal cell activity and injury, death, and genesis, which encompasses the modulation of structural and functional processes of axons, dendrites, and synapses. The range of structural elements that comprise plasticity includes long-term potentiation (a cellular correlate of learning and memory), synaptic efficacy and remodelling, synaptogenesis, axonal sprouting and dendritic remodelling, and neurogenesis and recruitment...
January 13, 2017: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/28077166/threonine-175-a-novel-pathological-phosphorylation-site-on-tau-protein-linked-to-multiple-tauopathies
#15
Alexander J Moszczynski, Wencheng Yang, Robert Hammond, Lee Cyn Ang, Michael J Strong
Microtubule associated protein tau (tau) deposition is associated with a spectrum of neurodegenerative diseases collectively termed tauopathies. We have previously shown that amyotrophic lateral sclerosis (ALS) with cognitive impairment (ALSci) is associated with tau phosphorylation at Thr(175) and that this leads to activation of GSK3β which then induces phosphorylation at tau Thr(231). This latter step leads to dissociation of tau from microtubules and pathological tau fibril formation. To determine the extent to which this pathway is unique to ALS, we have investigated the expression of pThr(175) tau and pThr(231) tau across a range of frontotemporal degenerations...
January 11, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28067492/the-polyphenol-altenusin-inhibits-in-vitro-fibrillization-of-tau-and-reduces-induced-tau-pathology-in-primary-neurons
#16
Sook Wern Chua, Alberto Cornejo, Janet van Eersel, Claire H Stevens, Inmaculada Vaca, Mercedes Cueto, Michael Kassiou, Amadeus Gladbach, Alex Macmillan, Lev Lewis, Renee Whan, Lars M Ittner
In Alzheimer's disease, the microtubule-associated protein tau forms intracellular neurofibrillary tangles (NFTs). A critical step in the formation of NFTs is the conversion of soluble tau into insoluble filaments. Accordingly, a current therapeutic strategy in clinical trials is aimed at preventing tau aggregation. Here, we assessed altenusin, a bioactive polyphenolic compound, for its potential to inhibit tau aggregation. Altenusin inhibits aggregation of tau protein into paired helical filaments in vitro...
January 12, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28053038/large-soluble-oligomers-of-amyloid-%C3%AE-protein-from-alzheimer-brain-are-far-less-neuroactive-than-the-smaller-oligomers-to-which-they-dissociate
#17
Ting Yang, Shaomin Li, Huixin Xu, Dominic M Walsh, Dennis J Selkoe
Soluble oligomers of amyloid β-protein (oAβ) isolated from the brains of Alzheimer's disease (AD) patients have been shown experimentally (in the absence of amyloid plaques) to impair hippocampal synaptic plasticity, decrease synapses, induce tau hyperphosphorylation and neuritic dystrophy, activate microglial inflammation, and impair memory in normal adult rodents. Nevertheless, there has been controversy about what types of oligomers actually confer these AD-like phenotypes. Here, we show that the vast majority of soluble Aβ species obtained from brains of humans who died with confirmed AD elute at high molecular weight (HMW) on nondenaturing size-exclusion chromatography...
January 4, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28035925/novel-phospho-tau-monoclonal-antibody-generated-using-a-liposomal-vaccine-with-enhanced-recognition-of-a-conformational-tauopathy-epitope
#18
Clara Theunis, Oskar Adolfsson, Natalia Crespo-Biel, Kasia Piorkowska, Maria Pihlgren, David T Hickman, Valérie Gafner, Peter Borghgraef, Herman Devijver, Andrea Pfeifer, Fred Van Leuven, Andreas Muhs
The microtubule-associated protein Tau is an intrinsically unfolded, very soluble neuronal protein. Under still unknown circumstances, Tau protein forms soluble oligomers and insoluble aggregates that are closely linked to the cause and progression of various brain pathologies, including Alzheimer's disease. Previously we reported the development of liposome-based vaccines and their efficacy and safety in preclinical mouse models for tauopathy. Here we report the use of a liposomal vaccine for the generation of a monoclonal antibody with particular characteristics that makes it a valuable tool for fundamental studies as well as a candidate antibody for diagnostic and therapeutic applications...
2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28009077/inflammasomes-as-therapeutic-targets-for-alzheimer-s-disease
#19
Claire S White, Catherine B Lawrence, David Brough, Jack Rivers-Auty
Alzheimer's disease is the most common form of progressive dementia, typified initially by short term memory deficits which develop into a dramatic global cognitive decline. The classical hall marks of Alzheimer's disease include the accumulation of amyloid oligomers and fibrils, and the intracellular formation of neurofibrillary tangles of hyperphosphorylated tau. It is now clear that inflammation also plays a central role in the pathogenesis of the disease through a number of neurotoxic mechanisms. Microglia are the key immune regulators of the CNS which detect amyloidopathy through cell surface and cytosolic pattern recognition receptors (PRRs) and respond by initiating inflammation through the secretion of cytokines such as interleukin-1β (IL-1β)...
March 2017: Brain Pathology
https://www.readbyqxmd.com/read/28006031/selection-and-characterization-of-tau-binding-%C3%A1-enantiomeric-peptides-with-potential-for-therapy-of-alzheimer-disease
#20
Christina Dammers, Deniz Yolcu, Laura Kukuk, Dieter Willbold, Marcus Pickhardt, Eckhard Mandelkow, Anselm H C Horn, Heinrich Sticht, Marwa Nidal Malhis, Nadja Will, Judith Schuster, Susanne Aileen Funke
A variety of neurodegenerative disorders, including Alzheimer disease (AD), are associated with neurofibrillary tangles composed of the tau protein, as well as toxic tau oligomers. Inhibitors of pathological tau aggregation, interrupting tau self-assembly, might be useful for the development of therapeutics. Employing mirror image phage display with a large peptide library (over 109 different peptides), we have identified tau fibril binding peptides consisting of d-enantiomeric amino acids. d-enantiomeric peptides are extremely protease stable and not or less immunogenic than l-peptides, and the suitability of d-peptides for in vivo applications have already been demonstrated...
2016: PloS One
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