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https://www.readbyqxmd.com/read/28453489/changes-of-cerebrospinal-fluid-peptides-due-to-tauopathy
#1
Petra Majerova, Peter Barath, Alena Michalicova, Stanislav Katina, Michal Novak, Andrej Kovac
Alzheimer's disease (AD) and progressive supranuclear palsy are two common neurodegenerative tauopathies, and the most common cause of progressive brain dementia in elderly affecting more than 35 million people. The tauopathies are characterized by abnormal deposition of microtubule associated protein tau into intracellular neurofibrillary tangles composed mainly of the hyperphosphorylated form of the protein. The diagnosis of tauopathies is based on the presence of clinical features and pathological changes...
April 27, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28434655/apolipoprotein-e-receptors-and-modulation-of-alzheimer-s-disease
#2
REVIEW
Na Zhao, Chia-Chen Liu, Wenhui Qiao, Guojun Bu
Apolipoprotein E (apoE) is a lipid carrier in both the peripheral and the central nervous systems. Lipid-loaded apoE lipoprotein particles bind to several cell surface receptors to support membrane homeostasis and injury repair in the brain. Considering prevalence and relative risk magnitude, the ε4 allele of the APOE gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD). ApoE4 contributes to AD pathogenesis by modulating multiple pathways, including but not limited to the metabolism, aggregation, and toxicity of amyloid-β peptide, tauopathy, synaptic plasticity, lipid transport, glucose metabolism, mitochondrial function, vascular integrity, and neuroinflammation...
March 14, 2017: Biological Psychiatry
https://www.readbyqxmd.com/read/28430857/repurposed-drugs-targeting-eif2%C3%AE-p-mediated-translational-repression-prevent-neurodegeneration-in-mice
#3
Mark Halliday, Helois Radford, Karlijn A M Zents, Collin Molloy, Julie A Moreno, Nicholas C Verity, Ewan Smith, Catharine A Ortori, David A Barrett, Martin Bushell, Giovanna R Mallucci
Signalling through the PERK/eIF2α-P branch of the unfolded protein response plays a critical role in controlling protein synthesis rates in cells. This pathway is overactivated in brains of patients with Alzheimer's disease and related disorders and has recently emerged as a promising therapeutic target for these currently untreatable conditions. Thus, in mouse models of neurodegenerative disease, prolonged overactivation of PERK/eIF2α-P signalling causes sustained attenuation of protein synthesis, leading to memory impairment and neuronal loss...
April 19, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28424326/anti-tau-antibody-administration-increases-plasma-tau-in-transgenic-mice-and-patients-with-tauopathy
#4
Kiran Yanamandra, Tirth K Patel, Hong Jiang, Suzanne Schindler, Jason D Ulrich, Adam L Boxer, Bruce L Miller, Diana R Kerwin, Gilbert Gallardo, Floy Stewart, Mary Beth Finn, Nigel J Cairns, Philip B Verghese, Ilana Fogelman, Tim West, Joel Braunstein, Grace Robinson, Jennifer Keyser, Joseph Roh, Stephanie S Knapik, Yan Hu, David M Holtzman
Tauopathies are a group of disorders in which the cytosolic protein tau aggregates and accumulates in cells within the brain, resulting in neurodegeneration. A promising treatment being explored for tauopathies is passive immunization with anti-tau antibodies. We previously found that administration of an anti-tau antibody to human tau transgenic mice increased the concentration of plasma tau. We further explored the effects of administering an anti-tau antibody on plasma tau. After peripheral administration of an anti-tau antibody to human patients with tauopathy and to mice expressing human tau in the central nervous system, there was a dose-dependent increase in plasma tau...
April 19, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/28420982/tau-oligomers-cytotoxicity-propagation-and-mitochondrial-damage
#5
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
#6
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/28416651/aav-mediated-expression-of-anti-tau-scfvs-decreases-tau-accumulation-in-a-mouse-model-of-tauopathy
#7
Christina Ising, Gilbert Gallardo, Cheryl E G Leyns, Connie H Wong, Floy Stewart, Lauren J Koscal, Joseph Roh, Grace O Robinson, Javier Remolina Serrano, David M Holtzman
Tauopathies are characterized by the progressive accumulation of hyperphosphorylated, aggregated forms of tau. Our laboratory has previously demonstrated that passive immunization with an anti-tau antibody, HJ8.5, decreased accumulation of pathological tau in a human P301S tau-expressing transgenic (P301S-tg) mouse model of frontotemporal dementia/tauopathy. To investigate whether the Fc domain of HJ8.5 is required for the therapeutic effect, we engineered single-chain variable fragments (scFvs) derived from HJ8...
April 17, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28416393/tdp-43-expression-influences-amyloid%C3%AE-plaque-deposition-and-tau-aggregation
#8
Stephani A Davis, Kok Ann Gan, James A Dowell, Nigel J Cairns, Michael A Gitcho
Although the main focus in Alzheimer's disease (AD) has been an investigation of mechanisms causing Aβ plaque deposition and tau tangle formation, recent studies have shown that phosphorylated TDP-43 pathology is present in up to 50% of sporadic cases. Furthermore, elevated phosphorylated TDP-43 has been associated with more severe AD pathology. Therefore, we hypothesized that TDP-43 may regulate amyloid-beta precursor protein (APP) trafficking and tau phosphorylation/aggregation. In order to examine the role of TDP-43 in AD, we developed a transgenic mouse that overexpresses hippocampal and cortical neuronal TDP-43 in a mouse expressing familial mutations (K595N and M596L) in APP and presenilin 1 (PSEN1ΔE9)...
April 20, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28413156/exposure-of-the-amino-terminus-of-tau-is-a-pathological-event-in-multiple-tauopathies
#9
Benjamin Combs, Nicholas M Kanaan
Pathological changes to the tau protein, including conformational changes and aggregation, are major hallmarks of a group of neurodegenerative disorders known as tauopathies. Among the conformational changes are alterations involving the extreme amino terminus of the protein, known as the phosphatase-activating domain (PAD). Aberrant PAD exposure induces a signaling cascade that leads to disruption of axonal transport, a critical function for neuronal survival. Conformational display of PAD is an early marker of pathological tau in Alzheimer disease (AD), but its role in other tauopathies has yet to be firmly established...
April 13, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28411086/early-depletion-of-ca1-neurons-and-late-neurodegeneration-in-a-mouse-tauopathy-model
#10
Lone Helboe, Jan Egebjerg, Pernille Barkholt, Christiane Volbracht
Alzheimer's disease (AD) and tauopathies, such as frontotemporal dementia (FTD), are characterized by formation of neurofibrillary tangles consisting of hyperphosphorylated tau. Further neuropathological characteristics include synaptic loss, neurodegeneration and brain atrophy. Here, we explored the association between hyperphosphorylated tau species, brain atrophy, synaptic and neuronal loss in a mouse model (rTg4510) carrying the human tau (hTau) P301L mutation found in a familiar form of FTD. We established that hTau expression during the first 6 postnatal weeks was important for the progression of tauopathy in rTg4510 mice...
April 11, 2017: Brain Research
https://www.readbyqxmd.com/read/28409749/the-role-of-stress-as-a-risk-factor-for-progressive-supranuclear-palsy
#11
Kristen D Kelley, Guerry Peavy, Steven Edland, Whitney Rogers, David E Riley, Yvette Bordelon, David Standaert, Stephen G Reich, Irene Litvan
BACKGROUND: PSP, like Alzheimer's disease (AD), is a tauopathy. The etiopathogenesis of PSP is not well known and the role of stress has not yet been examined. Recent studies have shown that stress increases the risk for developing AD. This study investigates the role of stress as a risk factor for PSP. OBJECTIVE: B To examine the association between the development of progressive supranuclear palsy (PSP) and self-reported life stressors. METHODS: 76 patients diagnosed with PSP according to the NINDS-SPSP criteria and 68 age-matched unrelated controls were administered a life stressor questionnaire...
April 13, 2017: Journal of Parkinson's Disease
https://www.readbyqxmd.com/read/28408879/comparison-of-in-vivo-and-ex-vivo-mri-for-the-detection-of-structural-abnormalities-in-a-mouse-model-of-tauopathy
#12
Holly E Holmes, Nick M Powell, Da Ma, Ozama Ismail, Ian F Harrison, Jack A Wells, Niall Colgan, James M O'Callaghan, Ross A Johnson, Tracey K Murray, Zeshan Ahmed, Morten Heggenes, Alice Fisher, M Jorge Cardoso, Marc Modat, Michael J O'Neill, Emily C Collins, Elizabeth M C Fisher, Sébastien Ourselin, Mark F Lythgoe
With increasingly large numbers of mouse models of human disease dedicated to MRI studies, compromises between in vivo and ex vivo MRI must be fully understood in order to inform the choice of imaging methodology. We investigate the application of high resolution in vivo and ex vivo MRI, in combination with tensor-based morphometry (TBM), to uncover morphological differences in the rTg4510 mouse model of tauopathy. The rTg4510 mouse also offers a novel paradigm by which the overexpression of mutant tau can be regulated by the administration of doxycycline, providing us with a platform on which to investigate more subtle alterations in morphology with morphometry...
2017: Frontiers in Neuroinformatics
https://www.readbyqxmd.com/read/28401333/interactions-of-pathological-proteins-in-neurodegenerative-diseases
#13
REVIEW
Tara L Spires-Jones, Johannes Attems, Dietmar Rudolf Thal
Neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal lobar degeneration (FTD), Lewy body disease (LBD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) have in common that protein aggregates represent pathological hallmark lesions. Amyloid β-protein, τ-protein, α-synuclein, and TDP-43 are the most frequently aggregated proteins in these disorders. Although they are assumed to form disease-characteristic aggregates, such as amyloid plaques and neurofibrillary tangles in AD or Lewy bodies in LBD/PD, they are not restricted to these clinical presentations...
April 11, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28400135/insulin-deficiency-results-in-reversible-protein-kinase-a-activation-and-tau-phosphorylation
#14
Judith M van der Harg, Leslie Eggels, Fabian N Bangel, Silvie R Ruigrok, Rob Zwart, Jeroen J M Hoozemans, Susanne E la Fleur, Wiep Scheper
Alzheimer's disease (AD) is a highly prevalent multifactorial disease for which Diabetes Mellitus (DM) is a risk factor. Abnormal phosphorylation and aggregation of tau is a key hallmark of AD. In animal models, DM induces or exacerbates the phosphorylation of tau, suggesting that DM may influence the risk at AD by directly facilitating tau pathology. Previously we reported that tau phosphorylation induced in response to metabolic stress is reversible. Since identification and understanding of early players in tau pathology is pivotal for therapeutic intervention, we here investigated the mechanism underlying tau phosphorylation in the diabetic brain and its potential for reversibility...
April 8, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28386764/roles-of-tau-protein-in-health-and-disease
#15
REVIEW
Tong Guo, Wendy Noble, Diane P Hanger
Tau is well established as a microtubule-associated protein in neurons. However, under pathological conditions, aberrant assembly of tau into insoluble aggregates is accompanied by synaptic dysfunction and neural cell death in a range of neurodegenerative disorders, collectively referred to as tauopathies. Recent advances in our understanding of the multiple functions and different locations of tau inside and outside neurons have revealed novel insights into its importance in a diverse range of molecular pathways including cell signalling, synaptic plasticity, and regulation of genomic stability...
May 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28382615/a-case-of-multiple-system-atrophy-with-preexisting-alzheimer-s-disease-and-predating-the-hot-cross-bun-sign
#16
Chi-Wei Lin, Chi-Yu Tseng, Chung-Ping Lo, Min-Chien Tu
PURPOSE: Synucleinopathy, tauopathy and amyloidopathy were classified as distinct clinical and pathological entities in traditional classification systems, and their interactions have been studied on neuropathology and molecular genetics recently. CASE REPORT: In this report, we present a 69-year-old male patient who had been diagnosed with probable Alzheimer's disease (AD) dementia due to progressive forgetfulness in February 2013. His Mini- Mental State Examination score was 21/30, and his Cognitive Abilities Screening Instrument score was 78/100, resulted from profound deficits in recent memory and abstract thinking domains...
December 15, 2016: Acta Neurologica Taiwanica
https://www.readbyqxmd.com/read/28382304/tau-oligomers-in-cerebrospinal-fluid-in-alzheimer-s-disease
#17
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/28379300/combined-effects-of-scanning-ultrasound-and-a-tau-specific-single-chain-antibody-in-a-tau-transgenic-mouse-model
#18
Rebecca M Nisbet, Ann Van der Jeugd, Gerhard Leinenga, Harrison T Evans, Phillip W Janowicz, Jürgen Götz
Alzheimer's disease is characterized by the deposition of amyloid-β as extracellular plaques and hyperphosphorylated tau as intracellular neurofibrillary tangles. Tau pathology characterizes not only Alzheimer's disease, but also many other tauopathies, presenting tau as an attractive therapeutic target. Passive tau immunotherapy has been previously explored; however, because only a small fraction of peripherally delivered antibodies crosses the blood-brain barrier, enters the brain and engages with tau that forms intracellular aggregates, more efficient ways of antibody delivery and neuronal uptake are warranted...
March 4, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28377597/dyrk1a-overexpression-leads-to-increase-of-3r-tau-expression-and-cognitive-deficits-in-ts65dn-down-syndrome-mice
#19
Xiaomin Yin, Nana Jin, Jianhua Shi, Yanchong Zhang, Yue Wu, Cheng-Xin Gong, Khalid Iqbal, Fei Liu
Alternative splicing of tau exon 10 generates tau isoforms with three or four microtubule-binding repeats, 3R-tau and 4R-tau, which is equally expressed in adult human brain. Imbalanced expression in 3R-tau and 4R-tau has been found in several sporadic and inherited tauopathies, suggesting that dysregulation of tau exon 10 is sufficient to cause neurodegenerative diseases. We previously reported that Dyrk1A, which is overexpressed in Down syndrome brains, regulates alternative splicing of exogenous tau exon 10...
April 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28370398/tau-aggregates-where-when-why-and-what-consequences
#20
EDITORIAL
Matthew P Frosch
Neuropathologists have been aware of neurofibrillary tangles for more than a century following their description as part of Alois Alzheimer's initial report. Since those early days, our understanding of the relationship of this particular type of cellular inclusion associated with neurodegeneration has continually broadened. Textbooks, now a partially antiquated concept, commonly list a range of disorders as being associated with tangles -NDASH- including typical neurodegenerative diseases (Alzheimer disease [AD], forms of frontotemporal lobar degenerations [FTLD-tau], progressive supranuclear palsy [PSP], corticobasal degeneration [CBD], primary aged related tauopathy [PART]), secondary degenerative diseases such as chronic traumatic encephalopathy, metabolic disease (Niemann-Pick disease type C) and infections (SSPE)...
April 2, 2017: Neuropathology and Applied Neurobiology
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