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https://www.readbyqxmd.com/read/27924507/tppu-protects-tau-from-h2o2-induced-hyperphosphorylation-in-hek293-tau-cells-by-regulating-pi3k-akt-gsk-3%C3%AE-pathway
#1
En-Sheng Yao, Yan Tang, Xing-Hua Liu, Ming-Huan Wang
Neurofibrillary pathology of abnormally hyperphosphorylated tau is a hallmark of Alzheimer's disease (AD) and other tauopathies. Phosphatidylinositol 3-kinase (PI3K)/Akt/glycogen synthase kinase-3 beta (GSK-3β) signaling pathway is pivotal for tau phosphorylation. Inhibition of soluble epoxide hydrolase (sEH) metabolism has been shown to effectively increase the accumulation of epoxyeicosatrienoic acids (EETs), which are cytochrome P450 metabolites of arachidonic acid and have been demonstrated to have neuroprotective effects...
December 2016: Journal of Huazhong University of Science and Technology. Medical Sciences
https://www.readbyqxmd.com/read/27911827/tau-prions-from-alzheimer-s-disease-and-chronic-traumatic-encephalopathy-patients-propagate-in-cultured-cells
#2
Amanda L Woerman, Atsushi Aoyagi, Smita Patel, Sabeen A Kazmi, Iryna Lobach, Lea T Grinberg, Ann C McKee, William W Seeley, Steven H Olson, Stanley B Prusiner
Tau prions are thought to aggregate in the central nervous system, resulting in neurodegeneration. Among the tauopathies, Alzheimer's disease (AD) is the most common, whereas argyrophilic grain disease (AGD), corticobasal degeneration (CBD), chronic traumatic encephalopathy (CTE), Pick's disease (PiD), and progressive supranuclear palsy (PSP) are less prevalent. Brain extracts from deceased individuals with PiD, a neurodegenerative disorder characterized by three-repeat (3R) tau prions, were used to infect HEK293T cells expressing 3R tau fused to yellow fluorescent protein (YFP)...
November 28, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27911749/casting-a-wide-net-role-of-perineuronal-nets-in-neural-plasticity
#3
Barbara A Sorg, Sabina Berretta, Jordan M Blacktop, James W Fawcett, Hiroshi Kitagawa, Jessica C F Kwok, Marta Miquel
Perineuronal nets (PNNs) are unique extracellular matrix structures that wrap around certain neurons in the CNS during development and control plasticity in the adult CNS. They appear to contribute to a wide range of diseases/disorders of the brain, are involved in recovery from spinal cord injury, and are altered during aging, learning and memory, and after exposure to drugs of abuse. Here the focus is on how a major component of PNNs, chondroitin sulfate proteoglycans, control plasticity, and on the role of PNNs in memory in normal aging, in a tauopathy model of Alzheimer's disease, and in drug addiction...
November 9, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27910888/microtubule-stabilising-peptides-rescue-tau-phenotypes-in-vivo
#4
Shmma Quraishe, Megan Sealey, Louise Cranfield, Amritpal Mudher
The microtubule cytoskeleton is a highly dynamic, filamentous network underpinning cellular structure and function. In Alzheimer's disease, the microtubule cytoskeleton is compromised, leading to neuronal dysfunction and eventually cell death. There are currently no disease-modifying therapies to slow down or halt disease progression. However, microtubule stabilisation is a promising therapeutic strategy that is being explored. We previously investigated the disease-modifying potential of a microtubule-stabilising peptide NAP (NAPVSIPQ) in a well-established Drosophila model of tauopathy characterised by microtubule breakdown and axonal transport deficits...
December 2, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27902456/long-term-caloric-restriction-in-apoe-deficient-mice-results-in-neuroprotection-via-fgf21-induced-ampk-mtor-pathway
#5
Claire Rühlmann, Tjark Wölk, Tobias Blümel, Laura Stahn, Brigitte Vollmar, Angela Kuhla
Caloric restriction (CR) decelerates the aging process, extends lifespan and exerts neuroprotective effects in diverse species by so far unknown mechanisms. Based on known neuroprotective effects of fibroblastic growth factor 21 (Fgf21) we speculate that CR upregulates Fgf21, which phosphorylates neuronal AMP-activated protein kinase (AMPK), leading to a decrease of mammalian target of rapamycin (mTOR) signaling activity and an inhibition of tau-hyperphosphorylation. This in turn reduces the formation of neurofibrillary tangles, a neuropathological hallmark of Alzheimer´s disease...
November 29, 2016: Aging
https://www.readbyqxmd.com/read/27890528/pathological-concentration-of-zinc-dramatically-accelerates-abnormal-aggregation-of-full-length-human-tau-and-thereby-significantly-increases-tau-toxicity-in-neuronal-cells
#6
Ji-Ying Hu, De-Lin Zhang, Xiao-Ling Liu, Xue-Shou Li, Xiao-Qing Cheng, Jie Chen, Hai-Ning Du, Yi Liang
A pathological hallmark of Alzheimer disease and other tauopathies is the formation of neurofibrillary tangles mainly composed of bundles of fibrils formed by microtubule-associated protein Tau. Here we study the effects of Zn(2+) on abnormal aggregation and cytotoxicity of a pathological mutant ΔK280 of full-length human Tau. As revealed by Congo red binding assays, transmission electron microscopy, immunofluorescence, Western blot, and immunogold electron microscopy, pathological concentration of Zn(2+) dramatically accelerates the fibrillization of ΔK280 both in vitro and in SH-SY5Y neuroblastoma cells...
November 23, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27878758/gender-specific-expression-of-ubiquitin-specific-peptidase-9-modulates-tau-expression-and-phosphorylation-possible-implications-for-tauopathies
#7
Sandra Köglsberger, Maria Lorena Cordero-Maldonado, Paul Antony, Julia Ilona Forster, Pierre Garcia, Manuel Buttini, Alexander Crawford, Enrico Glaab
Public transcriptomic studies have shown that several genes display pronounced gender differences in their expression in the human brain, which may influence the manifestations and risk for neuronal disorders. Here, we apply a transcriptome-wide analysis to discover genes with gender-specific expression and significant alterations in public postmortem brain tissue from Alzheimer's disease (AD) patients compared to controls. We identify the sex-linked ubiquitin-specific peptidase 9 (USP9) as an outstanding candidate gene with highly significant expression differences between the genders and male-specific underexpression in AD...
November 23, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27878366/widespread-tau-seeding-activity-at-early-braak-stages
#8
Jennifer L Furman, Jaime Vaquer-Alicea, Charles L White, Nigel J Cairns, Peter T Nelson, Marc I Diamond
Transcellular propagation of tau aggregates may underlie the progression of pathology in Alzheimer's disease (AD) and other tauopathies. Braak staging (B1, B2, B3) is based on phospho-tau accumulation within connected brain regions: entorhinal cortex (B1); hippocampus/limbic system (B2); and frontal and parietal lobes (B3). We previously developed a specific and sensitive assay that uses flow cytometry to quantify tissue seeding activity based on fluorescence resonance energy transfer (FRET) in cells that stably express tau reporter proteins...
November 22, 2016: Acta Neuropathologica
https://www.readbyqxmd.com/read/27861346/unusual-phenotype-of-pathologically-confirmed-progressive-supranuclear-palsy-with-autonomic-dysfunction-and-cerebellar-ataxia-case-report
#9
Katerina Mensikova, Lucie Tuckova, Jiri Ehrmann, Petr Kanovsky
BACKGROUND: Based on the results of recent multicenter clinical-pathological studies, it seems that the clinical heterogeneity of progressive supranuclear palsy (PSP) is much broader than previously thought. We will report 2 cases of patients with unusual manifestation of pathologically confirmed PSP. METHODS: Two female patients were diagnosed with the parkinsonian phenotype of multiple system atrophy (MSAP) according to current clinical diagnostic criteria at the ages of 55 and 60 years, respectively...
November 2016: Medicine (Baltimore)
https://www.readbyqxmd.com/read/27859539/clinicopathologic-heterogeneity-in-ftdp-17-due-to-mapt-p-p301l-mutation-including-a-patient-with-globular-glial-tauopathy
#10
Pawel Tacik, Monica Sanchez-Contreras, Michael DeTure, Melissa E Murray, Rosa Rademakers, Owen A Ross, Zbigniew K Wszolek, Joseph E Parisi, David S Knopman, Ronald C Petersen, Dennis W Dickson
AIM: The p.P301L mutation in microtubule-associated protein tau (MAPT) is a common cause of frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17). We compare clinicopathologic features of five unrelated and three related (brother, sister and cousin) patients with FTDP-17 due to p.P301L mutation. METHODS: Genealogical, clinical, neuropathologic, and genetic data were reviewed from eight individuals RESULTS: The series consisted of five men and three women with an average age of death of 58 years (52-65 years) and average disease duration of 9 years (3-14 years)...
November 8, 2016: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/27819070/primary-age-related-tauopathy-and-the-amyloid-cascade-hypothesis-the-exception-that-proves-the-rule
#11
John F Crary
Extensive data supports the amyloid cascade hypothesis, which states that Alzheimer's disease (AD) stems from neurotoxic forms of the amyloid-beta (Aβ) peptide. But the poor correlation between Aβ plaques and neurodegeneration/cognitive impairment, the spaciotemporal disparity between Aβ and tau pathology, and the disappointing results following several large clinical trials using Aβ-targeting agents are inconsistent with this explanation. The most perplexing inconsistency is the existence of AD-type dementia patients that develop abundant neurofibrillary tangles that are indistinguishable from those in early to moderate-stage AD in the absence of compelling evidence of amyloid toxicity...
2016: Journal of Neurology & Neuromedicine
https://www.readbyqxmd.com/read/27818384/hippocampal-t-cell-infiltration-promotes-neuroinflammation-and-cognitive-decline-in-a-mouse-model-of-tauopathy
#12
Cyril Laurent, Guillaume Dorothée, Stéphane Hunot, Elodie Martin, Yann Monnet, Marie Duchamp, Yuan Dong, François-Pierre Légeron, Antoine Leboucher, Sylvie Burnouf, Emilie Faivre, Kévin Carvalho, Raphaëlle Caillierez, Nadège Zommer, Dominique Demeyer, Nathalie Jouy, Veronique Sazdovitch, Susanna Schraen-Maschke, Cécile Delarasse, Luc Buée, David Blum
Alzheimer's disease is characterized by the combined presence of amyloid plaques and tau pathology, the latter being correlated with the progression of clinical symptoms. Neuroinflammatory changes are thought to be major contributors to Alzheimer's disease pathophysiology, even if their precise role still remains largely debated. Notably, to what extent immune responses contribute to cognitive impairments promoted by tau pathology remains poorly understood. To address this question, we took advantage of the THY-Tau22 mouse model that progressively develops hippocampal tau pathology paralleling cognitive deficits and reappraised the interrelationship between tau pathology and brain immune responses...
November 5, 2016: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/27814296/early-evidence-of-low-bone-density-and-decreased-serotonergic-synthesis-in-the-dorsal-raphe-of-a%C3%A2-tauopathy-model-of-alzheimer-s-disease
#13
Christine M Dengler-Crish, Matthew A Smith, Gina N Wilson
Reduced bone mineral density (BMD) and its clinical sequelae, osteoporosis, occur at a much greater rate the rate in patients with Alzheimer's disease (AD), often emerging early in the disease before significant cognitive decline is seen. Reduced BMD translates to increased bone fracture risk, decreased quality of life, and increased mortality for AD patients. However, the mechanism responsible for this observation is unclear. We hypothesize that bone loss is an additional component of an AD prodrome, changes that emerge prior to dementia and are mediated by dysfunction of the central serotonergic pathways...
November 3, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/27810929/unique-pathological-tau-conformers-from-alzheimer-s-brains-transmit-tau-pathology-in-nontransgenic-mice
#14
Jing L Guo, Sneha Narasimhan, Lakshmi Changolkar, Zhuohao He, Anna Stieber, Bin Zhang, Ronald J Gathagan, Michiyo Iba, Jennifer D McBride, John Q Trojanowski, Virginia M Y Lee
Filamentous tau aggregates are hallmark lesions in numerous neurodegenerative diseases, including Alzheimer's disease (AD). Cell culture and animal studies showed that tau fibrils can undergo cell-to-cell transmission and seed aggregation of soluble tau, but this phenomenon was only robustly demonstrated in models overexpressing tau. In this study, we found that intracerebral inoculation of tau fibrils purified from AD brains (AD-tau), but not synthetic tau fibrils, resulted in the formation of abundant tau inclusions in anatomically connected brain regions in nontransgenic mice...
November 14, 2016: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/27793194/activation-of-the-unfolded-protein-response-and-granulovacuolar-degeneration-are-not-common-features-of-human-prion-pathology
#15
Vera I Wiersma, Wim van Hecke, Wiep Scheper, Martijn A J van Osch, Will J M Hermsen, Annemieke J M Rozemuller, Jeroen J M Hoozemans
Human prion diseases are fatal neurodegenerative disorders with a genetic, sporadic or infectiously acquired aetiology. Neuropathologically, human prion diseases are characterized by deposition of misfolded prion protein and neuronal loss. In post-mortem brain tissue from patients with other neurodegenerative diseases characterized by protein misfolding, including Alzheimer's disease (AD) and frontotemporal lobar degeneration with tau pathology (FTLD-tau), increased activation of the unfolded protein response (UPR) has been observed...
October 28, 2016: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/27793193/hippocampal-phospho-tau-mapt-neuropathology-in-the-fornix-in-alzheimer-disease-an-immunohistochemical-autopsy-study
#16
Edward D Plowey, Jennifer L Ziskin
Whereas early Alzheimer disease (AD) neuropathology and mild cognitive impairment are relatively common in aging, accurate prediction of patients that will progress to dementia requires new biomarkers. Recently, substantial work has focused on phospho-tau/MAPT (p-MAPT) neuropathology since its regional propagation correlates with the degree of cognitive impairment in AD. Recent diffusion tensor imaging studies in AD suggest that increased diffusion in the fornix secondary to p-MAPT-related axonal injury could serve as a predictive biomarker of the risk of disease progression...
October 28, 2016: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/27787958/-18-f-av-1451-tau-positron-emission-tomography-in-progressive-supranuclear-palsy
#17
Jennifer L Whitwell, Val J Lowe, Nirubol Tosakulwong, Stephen D Weigand, Matthew L Senjem, Christopher G Schwarz, Anthony J Spychalla, Ronald C Petersen, Clifford R Jack, Keith A Josephs
BACKGROUND: The [(18) F]AV-1451 positron emission tomography ligand allows the in vivo assessment of tau proteins in the brain. It shows strong binding in Alzheimer's dementia, but little is known about how it performs in progressive supranuclear palsy, a primary 4R tauopathy. OBJECTIVES: The objectives of this study were to determine whether [(18) F]AV-1451 uptake can be observed in progressive supranuclear palsy and to characterize the regional distribution when compared with controls and Alzheimer's dementia...
October 27, 2016: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/27781973/magnetic-resonance-imaging-and-positron-emission-tomography-in-the-diagnosis-of-neurodegenerative-dementias
#18
A Del Sole, S Malaspina, Alberto Magenta Biasina
Neuroimaging, both with magnetic resonance imaging (MRI) and positron emission tomography (PET), has gained a pivotal role in the diagnosis of primary neurodegenerative diseases. These two techniques are used as biomarkers of both pathology and progression of Alzheimer's disease (AD) and to differentiate AD from other neurodegenerative diseases. MRI is able to identify structural changes including patterns of atrophy characterizing neurodegenerative diseases, and to distinguish these from other causes of cognitive impairment, e...
October 26, 2016: Functional Neurology
https://www.readbyqxmd.com/read/27770214/clustering-of-tau-immunoreactive-pathology-in-chronic-traumatic-encephalopathy
#19
Richard A Armstrong, Ann C McKee, Victor E Alvarez, Nigel J Cairns
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder which may result from repetitive brain injury. A variety of tau-immunoreactive pathologies are present, including neurofibrillary tangles (NFT), neuropil threads (NT), dot-like grains (DLG), astrocytic tangles (AT), and occasional neuritic plaques (NP). In tauopathies, cellular inclusions in the cortex are clustered within specific laminae, the clusters being regularly distributed parallel to the pia mater. To determine whether a similar spatial pattern is present in CTE, clustering of the tau-immunoreactive pathology was studied in the cortex, hippocampus, and dentate gyrus in 11 cases of CTE and 7 cases of Alzheimer's disease neuropathologic change (ADNC) without CTE...
October 21, 2016: Journal of Neural Transmission
https://www.readbyqxmd.com/read/27760426/cl-nqtrp-alleviates-tauopathy-symptoms-in-a-model-organism-through-the-inhibition-of-tau-aggregation-engendered-toxicity
#20
Moran Frenkel-Pinter, Sharon Tal, Roni Scherzer-Attali, Malak Abu-Hussien, Idan Alyagor, Tal Eisenbaum, Ehud Gazit, Daniel Segal
Alzheimer's disease (AD) is the most abundant tauopathy and is characterized by Aβ-derived plaques and tau-derived tangles, resulting from the unfolding of the corresponding monomeric subunits into ordered β-sheet oligomers and fibrils. Intervening in the toxic aggregation process is a promising therapeutic approach, but, to date, a disease-modifying therapy is neither available for AD nor for other tauopathies. Along these lines, we have previously demonstrated that a small naphthoquinone-tryptophan hybrid, termed NQTrp, is an effective modulator of tauopathy in vitro and in vivo...
October 20, 2016: Neuro-degenerative Diseases
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