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https://www.readbyqxmd.com/read/28620833/assessment-of-serum-uric-acid-as-risk-factor-for-tauopathies
#1
Tommaso Schirinzi, Giulia Di Lazzaro, Vito Luigi Colona, Paola Imbriani, Mohammad Alwardat, Giulia Maria Sancesario, Alessandro Martorana, Antonio Pisani
Low levels of serum uric acid (UA) are a risk factor for many neurodegenerative diseases but the role of UA in tauopathies has not been yet fully evaluated. In this study, we assessed the risk associated with serum UA levels in a large group of patients with tauopathies, either primary or secondary. The mean serum UA concentrations of 111 patients with tauopathies (TAU), including 41 with progressive supranuclear palsy (PSP), 45 with Alzheimer's disease (AD) and 25 with frontotemporal dementia (FTD) were compared to that of 130 controls (CTL)...
June 15, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/28610892/novel-human-neuronal-tau-model-exhibiting-neurofibrillary-tangles-and-transcellular-propagation
#2
Patrick Reilly, Charisse N Winston, Kelsey Baron, Margarita Trejo, Edward M Rockenstein, Johnny C Akers, Najla Kfoury, Marc Diamond, Eliezer Masliah, Robert A Rissman, Shauna H Yuan
Tauopathies are a class of neurodegenerative diseases, including Alzheimer's disease, frontotemporal dementia and progressive supranuclear palsy, that are associated with the pathological aggregation of tau protein in neurofibrillary tangles (NFT). Studies have characterized tau as a "prion-like" protein given its ability to form distinct, stable amyloid conformations capable of transcellular and multigenerational propagation in clonal fashion. It has been proposed that progression of tauopathy could be due to the prion-like propagation of tau, suggesting the possibility that end-stage pathologies like NFT formation may require an instigating event such as tau seeding...
June 10, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28605382/assessment-of-spontaneous-alternation-novel-object-recognition-and-limb-clasping-in-transgenic-mouse-models-of-amyloid-%C3%AE-and-tau-neuropathology
#3
Christian J Miedel, Jennifer M Patton, Andrew N Miedel, Edward S Miedel, Jonathan M Levenson
Here we describe a staged, behavioral testing approach that can be used to screen for compounds that exhibit in vivo efficacy on cognitive and functional motor behaviors in transgenic mouse models of β-amyloidosis and tauopathy. The paradigm includes tests for spontaneous alternation in a Y-maze, novel object recognition, and limb clasping. These tests were selected because they: 1) interrogate function of cognitive or motor domains and the correlate neural circuitry relevant to the human disease state, 2) have clearly defined endpoints, 3) have easily implementable quality control checks, 4) can be run in a moderate throughput format, and 5) require little intervention by the investigator...
May 28, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28600952/time-course-of-tau-toxicity-and-pharmacologic-prevention-in-a-cell%C3%A2-model-of-tauopathy
#4
Marcus Pickhardt, Jacek Biernat, Sabrina Hübschmann, Frank J A Dennissen, Thomas Timm, Annukka Aho, Eva-Maria Mandelkow, Eckhard Mandelkow
The aggregation of Tau protein is a hallmark of neurodegenerative diseases including Alzheimer's disease. Previously, we generated a cell model of tauopathy based on the 4-repeat domain with the FTDP-17 mutation ΔK280 (Tau(4RDΔK)) which is expressed in a regulatable fashion (tet-on). The deletion variant ΔK280 is highly amyloidogenic and forms fibrous aggregates in neuroblastoma N2a cells staining with the reporter dye Thioflavin S. The aggregation of Tau(4RDΔK) is toxic, contrary to wildtype or anti-aggregant variants of the protein...
May 3, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28599675/ykl-40-chitinase-3-like-i-is-expressed-in-a-subset-of-astrocytes-in-alzheimer-s-disease-and-other-tauopathies
#5
Marta Querol-Vilaseca, Martí Colom-Cadena, Jordi Pegueroles, Carla San Martín-Paniello, Jordi Clarimon, Olivia Belbin, Juan Fortea, Alberto Lleó
BACKGROUND: The innate immune system is known to be involved early in the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative disorders. The inflammatory response in the central nervous system can be measured postmortem or through a series of inflammatory mediator surrogates. YKL-40 (also named Chitinase-3-like I) has been frequently investigated in body fluids as a surrogate marker of neuroinflammation in AD and other neurological disorders. However, the expression pattern of YKL-40 in the human brain with neurodegenerative pathology remains poorly investigated...
June 9, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28591867/multisite-assessment-of-aging-related-tau-astrogliopathy-artag
#6
Gabor G Kovacs, Sharon X Xie, Edward B Lee, John L Robinson, Carrie Caswell, David J Irwin, Jon B Toledo, Victoria E Johnson, Douglas H Smith, Irina Alafuzoff, Johannes Attems, Janos Bencze, Kevin F Bieniek, Eileen H Bigio, Istvan Bodi, Herbert Budka, Dennis W Dickson, Brittany N Dugger, Charles Duyckaerts, Isidro Ferrer, Shelley L Forrest, Ellen Gelpi, Stephen M Gentleman, Giorgio Giaccone, Lea T Grinberg, Glenda M Halliday, Kimmo J Hatanpaa, Patrick R Hof, Monika Hofer, Tibor Hortobágyi, James W Ironside, Andrew King, Julia Kofler, Enikö Kövari, Jillian J Kril, Seth Love, Ian R Mackenzie, Qinwen Mao, Radoslav Matej, Catriona McLean, David G Munoz, Melissa E Murray, Janna Neltner, Peter T Nelson, Diane Ritchie, Roberta D Rodriguez, Zdenek Rohan, Annemieke Rozemuller, Kenji Sakai, Christian Schultz, Danielle Seilhean, Vanessa Smith, Pawel Tacik, Hitoshi Takahashi, Masaki Takao, Dietmar Rudolf Thal, Serge Weis, Stephen B Wharton, Charles L White, John M Woulfe, Masahito Yamada, John Q Trojanowski
Aging-related tau astrogliopathy (ARTAG) is a recently introduced terminology. To facilitate the consistent identification of ARTAG and to distinguish it from astroglial tau pathologies observed in the primary frontotemporal lobar degeneration tauopathies we evaluated how consistently neuropathologists recognize (1) different astroglial tau immunoreactivities, including those of ARTAG and those associated with primary tauopathies (Study 1); (2) ARTAG types (Study 2A); and (3) ARTAG severity (Study 2B). Microphotographs and scanned sections immunostained for phosphorylated tau (AT8) were made available for download and preview...
June 7, 2017: Journal of Neuropathology and Experimental Neurology
https://www.readbyqxmd.com/read/28587664/characterization-of-tau-prion-seeding-activity-and-strains-from-formaldehyde-fixed-tissue
#7
Sarah K Kaufman, Talitha L Thomas, Kelly Del Tredici, Heiko Braak, Marc I Diamond
Tauopathies such as Alzheimer's disease (AD) feature progressive intraneuronal deposition of aggregated tau protein. The cause is unknown, but in experimental systems trans-cellular propagation of tau pathology resembles prion pathogenesis. Tau aggregate inoculation into mice produces transmissible pathology, and tau forms distinct strains, i.e. conformers that faithfully replicate and create predictable patterns of pathology in vivo. The prion model predicts that tau seed formation will anticipate neurofibrillary tau pathology...
June 7, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28585382/modeling-tau-pathology-in-human-stem-cell-derived-neurons
#8
Selina Wray
Tau pathology is a defining characteristic of multiple neurodegenerative disorders including Alzheimer's disease (AD) and Frontotemporal Dementia (FTD) with tau pathology. There is strong evidence from genetics and experimental models to support a central role for tau dysfunction in neuronal death, suggesting tau is a promising therapeutic target for AD and FTD. However, the development of tau pathology can precede symptom onset by several years, so understanding the earliest molecular events in tauopathy is a priority area of research...
July 2017: Brain Pathology
https://www.readbyqxmd.com/read/28585125/role-of-microtubule-associated-protein-tau-phosphorylation-in-alzheimer-s-disease
#9
REVIEW
Rong-Hong Ma, Yao Zhang, Xiao-Yue Hong, Jun-Fei Zhang, Jian-Zhi Wang, Gong-Ping Liu
As a major microtubule-associated protein, tau plays an important role in promoting microtubule assembly and stabilizing microtubules. In Alzheimer's disease (AD) and other tauopathies, the abnormally hyperphosphorylated tau proteins are aggregated into paired helical filaments and accumulated in the neurons with the form of neurofibrillary tangles. An imbalanced regulation in protein kinases and protein phosphatases is the direct cause of tau hyperphosphorylation. Among various kinases and phosphatases, glycogen synthase kinase-3β (GSK-3β) and protein phosphatase 2A (PP2A) are the most implicated...
June 2017: Journal of Huazhong University of Science and Technology. Medical Sciences
https://www.readbyqxmd.com/read/28580182/cerebral-microvascular-accumulation-of-tau-oligomers-in-alzheimer-s-disease-and-related-tauopathies
#10
Diana L Castillo-Carranza, Ashley N Nilson, Candice E Van Skike, Jordan B Jahrling, Kishan Patel, Prajesh Garach, Julia E Gerson, Urmi Sengupta, Jose Abisambra, Peter Nelson, Juan Troncoso, Zoltan Ungvari, Veronica Galvan, Rakez Kayed
The importance of vascular contributions to cognitive impairment and dementia (VCID) associated with Alzheimer's disease (AD) and related neurodegenerative diseases is increasingly recognized, however, the underlying mechanisms remain obscure. There is growing evidence that in addition to Aβ deposition, accumulation of hyperphosphorylated oligomeric tau contributes significantly to AD etiology. Tau oligomers are toxic and it has been suggested that they propagate in a "prion-like" fashion, inducing endogenous tau misfolding in cells...
May 2017: Aging and Disease
https://www.readbyqxmd.com/read/28568506/pbb3-imaging-in-parkinsonian-disorders-evidence-for-binding-to-tau-and-other-proteins
#11
Alexandra Perez-Soriano, Julieta E Arena, Katie Dinelle, Qing Miao, Jessamyn McKenzie, Nicole Neilson, Andreas Puschmann, Paul Schaffer, Hitoshi Shinotoh, Jenna Smith-Forrester, Elham Shahinfard, Nasim Vafai, Daryl Wile, Zbigniew Wszolek, Makoto Higuchi, Vesna Sossi, A Jon Stoessl
BACKGROUND AND OBJECTIVES: To study selective regional binding for tau pathology in vivo, using PET with [(11) C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy. METHODS: Dynamic PET scans were obtained for 70 minutes after the bolus injection of [(11) C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region...
June 1, 2017: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/28558799/propagation-of-tau-aggregates
#12
REVIEW
Michel Goedert, Maria Grazia Spillantini
Since 2009, evidence has accumulated to suggest that Tau aggregates form first in a small number of brain cells, from where they propagate to other regions, resulting in neurodegeneration and disease. Propagation of Tau aggregates is often called prion-like, which refers to the capacity of an assembled protein to induce the same abnormal conformation in a protein of the same kind, initiating a self-amplifying cascade. In addition, prion-like encompasses the release of protein aggregates from brain cells and their uptake by neighbouring cells...
May 30, 2017: Molecular Brain
https://www.readbyqxmd.com/read/28552182/altered-protein-glycosylation-predicts-alzheimer-s-disease-and-modulates-its-pathology-in-disease-model-drosophila
#13
Moran Frenkel-Pinter, Shiri Stempler, Sharon Tal-Mazaki, Yelena Losev, Avnika Singh-Anand, Daniela Escobar-Álvarez, Jonathan Lezmy, Ehud Gazit, Eytan Ruppin, Daniel Segal
The pathological hallmarks of Alzheimer's disease (AD) are pathogenic oligomers and fibrils of misfolded amyloidogenic proteins (e.g., β-amyloid and hyper-phosphorylated tau in AD), which cause progressive loss of neurons in the brain and nervous system. Although deviations from normal protein glycosylation have been documented in AD, their role in disease pathology has been barely explored. Here our analysis of available expression data sets indicates that many glycosylation-related genes are differentially expressed in brains of AD patients compared with healthy controls...
May 3, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28550263/microglial-and-neuronal-tdp-43-pathology-in-anti-iglon5-related-tauopathy
#14
Annachiara Cagnin, Sara Mariotto, Michele Fiorini, Marina Gaule, Nicola Bonetto, Matteo Tagliapietra, Emanuele Buratti, Gianluigi Zanusso, Sergio Ferrari, Salvatore Monaco
A novel neuronal tauopathy, mainly confined to hypothalamus and brainstem tegmentum, has recently been reported in patients with autoantibodies to the neuronal cell-adhesion molecule IgLON5. We describe a patient with anti-IgLON5 syndrome, who presented with dysautonomia and sleep disorder, followed by subacute dementia. Postmortem brain examination disclosed neuronal tau pathology prevailing in the hippocampus, amygdala, and locus coeruleus, in addition to microglial/neuronal TDP-43 pathology, with overexpression of aberrantly phosphorylated forms and neurotoxic truncated fragments, in basal ganglia, nucleus basalis, thalamus, and midbrain...
May 26, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28544198/jaboticaba-berry-peel-intake-prevents-insulin-resistance-induced-tau-phosphorylation-in-mice
#15
Ângela G Batista, Edilene S Soares, Monique C P Mendonça, Juliana K da Silva, Ana Paula Dionísio, Cesar R Sartori, Maria Alice da Cruz-Höfling, Mário R Maróstica Júnior
The hyperphosphorylation of tau in the hippocampus can be caused by central and peripheral insulin resistance and these alterations are related to the development of tauopathies, such as Alzheimer's disease. In this study, we used a high-fat diet to induce obesity and insulin resistance in adult Swiss mice and checked whether supplementation with Myrciaria jaboticaba berry peel for 10 weeks could improve insulin sensitivity, learning/memory performance and prevent tau phosphorylation in the hippocampus. Furthermore, adipocytokines, inflammatory markers, and oxidative stress were assessed...
May 19, 2017: Molecular Nutrition & Food Research
https://www.readbyqxmd.com/read/28540657/uch-l1-inhibition-suppresses-tau-aggresome-formation-during-proteasomal-impairment
#16
Quntao Yu, Hongmao Zhang, Yuan Li, Chao Liu, Shaohui Wang, Xiaomei Liao
In conditions of proteasomal impairment, the damaged or misfolded proteins, collectively known as aggresome, can accumulate in the perinuclear space and be subsequently eliminated by autophagy. Abnormal aggregation of microtubule-associated protein tau in the cytoplasm is a common neuropathological feature of tauopathies. The deficiency in ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), a proteasomal deubiquitinating enzyme, is closely related to tau aggregation; however, the associated mechanisms remain unclear...
May 24, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28536263/axodendritic-sorting-and-pathological-missorting-of-tau-is-isoform-specific-and-determined-by-axon-initial-segment-architecture
#17
Hans Zempel, Frank Dennissen, Yatender Kumar, Julia Luedtke, Jacek Biernat, Eva-Maria Mandelkow, Eckhard Mandelkow
Subcellular mislocalization of the microtubule-associated protein Tau is a hallmark of Alzheimer disease (AD) and other tauopathies. Six Tau isoforms, differentiated by the presence or absence of a second repeat or of N-terminal inserts, exist in the human CNS but their physiological and pathological differences have long remained remain elusive. Here, we investigated the properties and distributions of human and rodent Tau isoforms in primary forebrain rodent neurons. We found that the Tau-Diffusion-Barrier (TDB), located within the Axon-Initial-Segment (AIS), controls retrograde (axon-to-soma) and anterograde (soma-to-axon) traffic of Tau...
May 23, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28536241/correction-aav-mediated-expression-of-anti-tau-scfvs-decreases-tau-accumulation-in-a-mouse-model-of-tauopathy
#18
Christina Ising, Gilbert Gallardo, Cheryl E G Leyns, Connie H Wong, Hong Jiang, Floy Stewart, Lauren J Koscal, Joseph Roh, Grace O Robinson, Javier Remolina Serrano, David M Holtzman
No abstract text is available yet for this article.
May 23, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28529046/targeted-downregulation-of-dmyc-restricts-neurofibrillary-tangles-mediated-pathogenesis-of-human-neuronal-tauopathies-in-drosophila
#19
Soram Idiyasan Chanu, Surajit Sarkar
Formation of Neurofibrillary Tangles (NFTs) in neuronal tissues has been implicated as the hallmark of disease pathogenesis and tau mediated toxicity in human and mammalian models. However, previous studies had failed to correlate NFT formation with pathogenesis of human neuronal tauopathies in Drosophila disease models. Though, a recent report suggests formation of tau mediated NFTs like structures confined to dopaminergic neurons in Drosophila adult brain, by utilizing various approaches, we demonstrate distinct and recurrent formation of NFTs in Drosophila neuronal tissues upon expression of wild type or mutant isoforms of human tau, and this appears as the key mediator of the pathogenesis of human neuronal tauopathy in Drosophila...
May 18, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28528968/amylin-and-its-g-protein-coupled-receptor-a-probable-pathological-process-and-drug-target-for-alzheimer-s-disease
#20
REVIEW
Wei Qiao Qiu
G-protein-coupled receptors (GPCRs) are shown to be involved in Alzheimer's disease (AD) pathogenesis. However, because GPCRs include a large family of membrane receptors, it is unclear which specific GPCR or pathway with rational ligands can become effective therapeutic targets for AD. Amylin receptor (AmR) is a GPCR that mediates several activities, such as improving glucose metabolism, relaxing cerebrovascular structure, modulating inflammatory reactions and potentially enhancing neural regeneration. Recent studies show that peripheral treatments with amylin or its clinical analog, pramlintide, reduced several components of AD pathology, including amyloid plaques, tauopathy, neuroinflammation and other components in the brain, corresponding with improved learning and memory in AD mouse models...
May 19, 2017: Neuroscience
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