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https://www.readbyqxmd.com/read/28205010/prion-specific-and-surrogate-csf-biomarkers-in-creutzfeldt-jakob-disease-diagnostic-accuracy-in-relation-to-molecular-subtypes-and-analysis-of-neuropathological-correlates-of-p-tau-and-a%C3%AE-42-levels
#1
Francesca Lattanzio, Samir Abu-Rumeileh, Alessia Franceschini, Hideaki Kai, Giulia Amore, Ilaria Poggiolini, Marcello Rossi, Simone Baiardi, Lynne McGuire, Anna Ladogana, Maurizio Pocchiari, Alison Green, Sabina Capellari, Piero Parchi
The differential diagnosis of Creutzfeldt-Jakob disease (CJD) from other, sometimes treatable, neurological disorders is challenging, owing to the wide phenotypic heterogeneity of the disease. Real-time quaking-induced prion conversion (RT-QuIC) is a novel ultrasensitive in vitro assay, which, at variance with surrogate neurodegenerative biomarker assays, specifically targets the pathological prion protein (PrP(Sc)). In the studies conducted to date in CJD, cerebrospinal fluid (CSF) RT-QuIC showed good diagnostic sensitivity (82-96%) and virtually full specificity...
February 15, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28202389/targeting-the-hdac2-hnf-4a-mir-101b-ampk-pathway-rescues-tauopathy-and-dendritic-abnormalities-in-alzheimer-s-disease
#2
Dan Liu, Hui Tang, Xin-Yan Li, Man-Fei Deng, Na Wei, Xiong Wang, Ya-Fan Zhou, Ding-Qi Wang, Peng Fu, Jian-Zhi Wang, Sébastien S Hébert, Jian-Guo Chen, Youming Lu, Ling-Qiang Zhu
Histone deacetylase 2 (HDAC2) plays a major role in the epigenetic regulation of gene expression. Previous studies have shown that HDAC2 expression is strongly increased in Alzheimer's disease (AD), a major neurodegenerative disorder and the most common form of dementia. Moreover, previous studies have linked HDAC2 to Aβ overproduction in AD; however, its involvement in tau pathology and other memory-related functions remains unclear. Here, we show that increased HDAC2 levels strongly correlate with phosphorylated tau in a mouse model of AD...
February 12, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28164774/tauopathies-focus-on-changes-at-the-neurovascular-unit
#3
Alena Michalicova, William A Banks, Jaroslav Legath, Andrej Kovac
In the past, the blood-brain barrier (BBB) had been characterized mainly as a layer of endothelial cells forming the vessel/capillary wall of the brain. More recently, the BBB is considered to be a part of a highly dynamic and interactive system called the neurovascular unit (NVU), consisting of vascular cells, glial cells, and neurons. The list of central nervous system (CNS) pathologies involving BBB dysfunction is rapidly growing. The opening of the BBB and subsequent infiltration of serum components to the brain can lead to host of processes resulting in progressive synaptic and neuronal dysfunction and loss...
February 3, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28160413/accelerated-aging-exacerbates-a-pre-existing-pathology-in-a-tau-transgenic-mouse-model
#4
Liviu-Gabriel Bodea, Harrison Tudor Evans, Ann Van der Jeugd, Lars M Ittner, Fabien Delerue, Jillian Kril, Glenda Halliday, John Hodges, Mathew C Kiernan, Jürgen Götz
Age is a critical factor in the prevalence of tauopathies, including Alzheimer's disease. To observe how an aging phenotype interacts with and affects the pathological intracellular accumulation of hyperphosphorylated tau, the tauopathy mouse model pR5 (expressing P301L mutant human tau) was back-crossed more than ten times onto a senescence-accelerated SAMP8 background to establish the new strain, SApT. Unlike SAMP8 mice, pR5 mice are characterized by a robust tau pathology particularly in the amygdala and hippocampus...
February 4, 2017: Aging Cell
https://www.readbyqxmd.com/read/28160067/tau-aggregation-influences-cognition-and-hippocampal-atrophy-in-the-absence-of-beta-amyloid-a-clinico-imaging-pathological-study-of-primary-age-related-tauopathy-part
#5
Keith A Josephs, Melissa E Murray, Nirubol Tosakulwong, Jennifer L Whitwell, David S Knopman, Mary M Machulda, Stephen D Weigand, Bradley F Boeve, Kejal Kantarci, Leonard Petrucelli, Val J Lowe, Clifford R Jack, Ronald C Petersen, Joseph E Parisi, Dennis W Dickson
We investigate whether there is any association between the Braak neurofibrillary tangle (NFT) stage and clinical and MRI features in definite primary age-related tauopathy (PART). We analysed 52 cases with a Braak NFT tangle stage >0 and ≤IV, and a Thal phase of 0 (no beta-amyloid present). Twenty-nine (56%) were female. Median age at death was 88 years (IQR 82-92 years). Fifteen (29%) were TDP-positive (75% TDP stage I), 16 (31%) had argyrophilic grain disease and three (6%) had alpha-synuclein-positive Lewy bodies...
February 3, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28159830/therapeutic-strategies-for-restoring-tau-homeostasis
#6
Zapporah T Young, Sue Ann Mok, Jason E Gestwicki
Normal tau homeostasis is achieved when the synthesis, processing, and degradation of the protein is balanced. Together, the pathways that regulate tau homeostasis ensure that the protein is at the proper levels and that its posttranslational modifications and subcellular localization are appropriately controlled. These pathways include the enzymes responsible for posttranslational modifications, those systems that regulate mRNA splicing, and the molecular chaperones that control tau turnover and its binding to microtubules...
February 3, 2017: Cold Spring Harbor Perspectives in Medicine
https://www.readbyqxmd.com/read/28157099/sex-impact-on-tau-aggregation-and-postsynaptic-protein-levels-in-the-p301l-mouse-model-of-tauopathy
#7
Lucia Buccarello, Giuliano Grignaschi, Anna Maria Castaldo, Alessia Di Giancamillo, Cinzia Domeneghini, Roberto Cosimo Melcangi, Tiziana Borsello
P301L transgenic (tg) mice well mimic features of human tauopathies and provide a good model for investigating the role of tau in neurodegenerative events. We here analyzed the possible interaction among phosphorylation of tau (p-tau), spine injury, neuronal death, and sex in the P301L mouse model of tauopathy. When compared to control mice (ctr), P301L transgenic mice (tg) presented with lower body weight, reduced survival rate, hyperphosphorylated tau, spine injury, and neuronal loss in both cerebral cortex and hippocampus at 15 months of age...
February 1, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28148553/perk-activation-mitigates-tau-pathology-in%C3%A2-vitro-and-in%C3%A2-vivo
#8
Julius Bruch, Hong Xu, Thomas W Rösler, Anderson De Andrade, Peer-Hendrik Kuhn, Stefan F Lichtenthaler, Thomas Arzberger, Konstanze F Winklhofer, Ulrich Müller, Günter U Höglinger
The RNA-like endoplasmic reticulum kinase (PERK) is genetically associated with the tauopathy progressive supranuclear palsy (PSP). To elucidate the functional mechanisms underlying this association, we explored PERK activity in brains of PSP patients and its function in three tauopathy models (cultured human neurons overexpressing 4-repeat wild-type tau or treated with the environmental neurotoxin annonacin, and P301S tau transgenic mice). In vitro, treatment with a pharmacological PERK activator CCT020312 or PERK overexpression reduced tau phosphorylation, tau conformational change and 4-repeat tau isoforms, and increased cell viability...
February 1, 2017: EMBO Molecular Medicine
https://www.readbyqxmd.com/read/28140402/glucose-deficit-triggers-tau-pathology-and-synaptic-dysfunction-in-a-tauopathy-mouse-model
#9
E Lauretti, J-G Li, A Di Meco, D Praticò
Clinical investigations have highlighted a biological link between reduced brain glucose metabolism and Alzheimer's disease (AD). Previous studies showed that glucose deprivation may influence amyloid beta formation in vivo but no data are available on the effect that this condition might have on tau protein metabolism. In the current paper, we investigated the effect of glucose deficit on tau phosphorylation, memory and learning, and synaptic function in a transgenic mouse model of tauopathy, the h-tau mice...
January 31, 2017: Translational Psychiatry
https://www.readbyqxmd.com/read/28138509/association-between-a%C3%AE-and-tau-accumulations-and-their-influence-on-clinical-features-in-aging-and-alzheimer-s-disease-spectrum-brains-a-11-c-pbb3-pet-study
#10
Hitoshi Shimada, Soichiro Kitamura, Hitoshi Shinotoh, Hironobu Endo, Fumitoshi Niwa, Shigeki Hirano, Yasuyuki Kimura, Ming-Rong Zhang, Satoshi Kuwabara, Tetsuya Suhara, Makoto Higuchi
INTRODUCTION: Amyloid-β (Aβ) and tau accumulations may occur independently and concurrently as exemplified by primary age-related tauopathy and Alzheimer's disease (AD), respectively. Interactions between Aβ and tau accumulations and their influence on clinical features, however, are still unclear. METHODS: Associations among clinical symptoms, gray-matter volume, regional tau, and Aβ deposition assessed by positron emission tomography with [(11)C]pyridinyl-butadienyl-benzothiazole 3 (PBB3) and [(11)C]Pittsburgh compound-B (PiB), were evaluated in 17 AD, 9 mild cognitive impairment due to AD, and 28 PiB(-)-cognitive healthy controls (HCs)...
2017: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
https://www.readbyqxmd.com/read/28138159/caspase-3-dependent-cleavage-of-akt-modulates-tau-phosphorylation-via-gsk3%C3%AE-kinase-implications-for-alzheimer-s-disease
#11
J Chu, E Lauretti, D Praticò
The pathological hallmark of Alzheimer's disease (AD) is accumulation of misfolded amyloid-β peptides and hyperphosphorylated tau protein in the brain. Increasing evidence suggests that serine-aspartyl proteases-caspases are activated in the AD brain. Previous studies identified a caspase-3 cleavage site within the amyloid-β precursor protein, and a caspase-3 cleavage of tau as the mechanisms involved in the development of Aβ and tau neuropathology, respectively. However, the potential role that caspase-3 could have on tau metabolism remains unknown...
January 31, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28130473/frontotemporal-dementia-with-the-v337m-mapt-mutation-tau-pet-and-pathology-correlations
#12
Salvatore Spina, Daniel R Schonhaut, Bradley F Boeve, William W Seeley, Rik Ossenkoppele, James P O'Neil, Andreas Lazaris, Howard J Rosen, Adam L Boxer, David C Perry, Bruce L Miller, Dennis W Dickson, Joseph E Parisi, William J Jagust, Melissa E Murray, Gil D Rabinovici
OBJECTIVE: To assess the efficacy of [(18)F]AV1451 PET in visualizing tau pathology in vivo in a patient with frontotemporal dementia (FTD) associated with the V337M microtubule-associated protein tau (MAPT) mutation. METHODS: MAPT mutations are associated with the deposition of hyperphosphorylated tau protein in neurons and glia. The PET tracer [(18)F]AV1451 binds with high affinity to paired helical filaments tau that comprises neurofibrillary tangles in Alzheimer disease (AD), while postmortem studies suggest lower or absent binding to the tau filaments of the majority of non-AD tauopathies...
January 27, 2017: Neurology
https://www.readbyqxmd.com/read/28129110/correcting-mir92a-vgat-mediated-gabaergic-dysfunctions-rescues-human-tau-induced-anxiety-in-mice
#13
Xiaoguang Li, Zhihao Wang, Lu Tan, Yali Wang, Chengbiao Lu, Rongxiang Chen, Shujuan Zhang, Yuan Gao, Yanchao Liu, Yaling Yin, Xinghua Liu, Enjie Liu, Ying Yang, Yu Hu, Zhipeng Xu, Fuqiang Xu, Jie Wang, Gong-Ping Liu, Jian-Zhi Wang
Patients with Alzheimer's disease (AD) commonly show anxiety behaviors, but the molecular mechanisms are not clear and no efficient intervention exists. Here, we found that overexpression of human wild-type, full-length tau (termed htau) in hippocampus significantly decreased the extracellular γ-aminobutyric acid (GABA) level with inhibition of γ oscillation and the evoked inhibitory postsynaptic potential (eIPSP). With tau accumulation, the mice show age-dependent anxiety behaviors. Among the factors responsible for GABA synthesis, release, uptake, and transport, we found that accumulation of htau selectively suppressed expression of the intracellular vesicular GABA transporter (vGAT)...
January 4, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28127516/serum-uric-acid-levels-in-parkinson-s-disease-and-related-disorders
#14
Hideki Sakuta, Keisuke Suzuki, Tomoyuki Miyamoto, Masayuki Miyamoto, Ayaka Numao, Hiroaki Fujita, Yuji Watanabe, Koichi Hirata
OBJECTIVE: Serum uric acid (UA) levels are reported to be decreased in patients with Parkinson's disease (PD) and multiple system atrophy (MSA). However, clinical correlates of serum UA levels are still unclear in PD-related disorders. We conducted a cross-sectional study to evaluate the associations between serum UA levels and disease duration, disease severity, and motor function among PD, MSA, and progressive supranuclear palsy (PSP) patients. METHODS: A total of 100 patients with PD, 42 patients with MSA, 30 patients with PSP, and 100 controls were included in this study...
January 2017: Brain and Behavior
https://www.readbyqxmd.com/read/28124562/a-two-component-adhesive-tau-fibrils-arise-from-a-combination-of-a-well-defined-motif-and-conformationally-flexible-interactions
#15
Shengqi Xiang, Natalia Kulminskaya, Birgit Habenstein, Jacek Biernat, Katharina Tepper, Maria Paulat, Christian Griesinger, Stefan Becker, Adam Lange, Eckhard Mandelkow, Rasmus Linser
Fibrillar aggregates of Aβ and Tau in the brain are the major hallmarks of Alzheimer's disease. Most Tau fibers have a twisted appearance, but the twist can be variable and even absent. This ambiguity, which has also been associated with different phenotypes of tauopathies, has led to controversial assumptions about fibril constitution, and it is unclear to-date what the molecular causes of this polymorphism are. To tackle this question, we used solid-state NMR strategies providing assignments of non-seeded three-repeat-domain Tau(3RD) with an inherent heterogeneity...
February 8, 2017: Journal of the American Chemical Society
https://www.readbyqxmd.com/read/28123067/tau-reduction-prevents-neuronal-loss-and-reverses-pathological-tau-deposition-and-seeding-in-mice-with-tauopathy
#16
Sarah L DeVos, Rebecca L Miller, Kathleen M Schoch, Brandon B Holmes, Carey S Kebodeaux, Amy J Wegener, Guo Chen, Tao Shen, Hien Tran, Brandon Nichols, Tom A Zanardi, Holly B Kordasiewicz, Eric E Swayze, C Frank Bennett, Marc I Diamond, Timothy M Miller
Accumulation of hyperphosphorylated tau directly correlates with cognitive decline in Alzheimer's disease and other primary tauopathies. One therapeutic strategy may be to reduce total tau expression. We identified antisense oligonucleotides (ASOs) that selectively decreased human tau mRNA and protein in mice expressing mutant P301S human tau. After reduction of human tau in this mouse model of tauopathy, fewer tau inclusions developed, and preexisting phosphorylated tau and Thioflavin S pathology were reversed...
January 25, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/28122879/18f-av-1451-positron-emission-tomography-in-alzheimer-s-disease-and-progressive-supranuclear-palsy
#17
Luca Passamonti, Patricia Vázquez Rodríguez, Young T Hong, Kieren S J Allinson, David Williamson, Robin J Borchert, Saber Sami, Thomas E Cope, W Richard Bevan-Jones, P Simon Jones, Robert Arnold, Ajenthan Surendranathan, Elijah Mak, Li Su, Tim D Fryer, Franklin I Aigbirhio, John T O'Brien, James B Rowe
The ability to assess the distribution and extent of tau pathology in Alzheimer's disease and progressive supranuclear palsy in vivo would help to develop biomarkers for these tauopathies and clinical trials of disease-modifying therapies. New radioligands for positron emission tomography have generated considerable interest, and controversy, in their potential as tau biomarkers. We assessed the radiotracer (18)F-AV-1451 with positron emission tomography imaging to compare the distribution and intensity of tau pathology in 15 patients with Alzheimer's pathology (including amyloid-positive mild cognitive impairment), 19 patients with progressive supranuclear palsy, and 13 age- and sex-matched controls...
January 24, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28119058/analysis-of-ribosomal-protein-s6-baseline-phosphorylation-and-effect-of-tau-pathology-in-the-murine-brain-and-human-hippocampus
#18
Maria Klingebiel, Maja Dinekov, Christoph Köhler
We examined the distribution pattern of the phosphorylated 40S ribosomal subunit protein S6, a downstream target of the mTOR pathway, in the brains of 24-months-old human tau transgenic pR5 mice, non-transgenic littermates and in human hippocampi. We studied baseline levels of phosphorylated S6 and a possible effect of tau pathology. S6 phosphorylated at Ser235/236 (pS6Ser235/236) or Ser240/244 (pS6Ser240/244) has been used as a read-out of mTOR activity in several studies. The mTOR pathway regulates a wide variety of cellular functions including cell growth, ribosome biosynthesis, translational control and autophagy...
January 21, 2017: Brain Research
https://www.readbyqxmd.com/read/28115743/adnp-nap-dramatically-increase-microtubule-end-binding-protein-tau-interaction-a-novel-avenue-for-protection-against-tauopathy
#19
Y Ivashko-Pachima, C Laura Sayas, A Malishkevich, I Gozes
Activity-dependent neuroprotective protein (ADNP), vital for brain formation and cognitive function, is mutated in autism and linked to neurodegenerative/psychiatric diseases. An eight-amino-acid peptide snippet of ADNP, NAP (NAPVSIPQ), identified as a smallest active fragment, includes the SxIP microtubule (MT) end-binding protein (EB) association motif, and enhances ADNP-EB3 interaction. Depletion of EB1 or EB3 abolishes NAP protection against zinc intoxication. Furthermore, NAP enhances Tau-MT interaction, and Tau regulates the localization and function of EB1 and EB3 in developing neuronal cells...
January 24, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28112682/nasal-neuron-pet-imaging-quantifies-neuron-generation-and-degeneration
#20
Genevieve C Van de Bittner, Misha M Riley, Luxiang Cao, Janina Ehses, Scott P Herrick, Emily L Ricq, Hsiao-Ying Wey, Michael J O'Neill, Zeshan Ahmed, Tracey K Murray, Jaclyn E Smith, Changning Wang, Frederick A Schroeder, Mark W Albers, Jacob M Hooker
Olfactory dysfunction is broadly associated with neurodevelopmental and neurodegenerative diseases and predicts increased mortality rates in healthy individuals. Conventional measurements of olfactory health assess odor processing pathways within the brain and provide a limited understanding of primary odor detection. Quantification of the olfactory sensory neurons (OSNs), which detect odors within the nasal cavity, would provide insight into the etiology of olfactory dysfunction associated with disease and mortality...
February 1, 2017: Journal of Clinical Investigation
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