Journal articles: 'Tau Effect'

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Kawabe, Takahiro, Kayo Miura, and Yuki Yamada. "Audiovisual tau effect." Acta Psychologica 128, no. 2 (June 2008): 249–54. http://dx.doi.org/10.1016/j.actpsy.2008.01.004.

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Barthelemy, Nicolas R., Haiyan Liu, Randall Bateman, and Brendan P. Lucey. "P4-066: EFFECT OF SLEEP ON CSF TAU AND P-TAU." Alzheimer's & Dementia 15 (July 2019): P1298. http://dx.doi.org/10.1016/j.jalz.2019.06.3726.

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Barthelemy, Nicolas R., Haiyan Liu, Randall Bateman, and Brendan P. Lucey. "F2-08-03: EFFECT OF SLEEP ON CSF TAU AND P-TAU." Alzheimer's & Dementia 15 (July 2019): P529—P530. http://dx.doi.org/10.1016/j.jalz.2019.06.4446.

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Das, Rashmi, Abhishek Ankur Balmik, and Subashchandrabose Chinnathambi. "Effect of Melatonin on Tau aggregation and Tau-mediated cell surface morphology." International Journal of Biological Macromolecules 152 (June 2020): 30–39. http://dx.doi.org/10.1016/j.ijbiomac.2020.01.296.

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Kawabe, Takahiro, Nobu Shirai, Yuji Wada, Kayo Miura, So Kanazawa, and Masami K. Yamaguchi. "The Audiovisual Tau Effect in Infancy." PLoS ONE 5, no. 3 (March 3, 2010): e9503. http://dx.doi.org/10.1371/journal.pone.0009503.

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Gil, Laura, Concetta Federico, Fernando Pinedo, Francesca Bruno, Ana B. Rebolledo, Juan J. Montoya, Isabel M. Olazabal, Isidre Ferrer, and Salvatore Saccone. "Aging dependent effect of nuclear tau." Brain Research 1677 (December 2017): 129–37. http://dx.doi.org/10.1016/j.brainres.2017.09.030.

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Liu, Guanghao, Ramasamy Thangavel, Jacob Rysted, Yohan Kim, Meghan B. Francis, Eric Adams, Zhihong Lin, et al. "Loss of tau and Fyn reduces compensatory effects of MAP2 for tau and reveals a Fyn‐independent effect of tau on calcium." Journal of Neuroscience Research 97, no. 11 (August 26, 2019): 1393–413. http://dx.doi.org/10.1002/jnr.24517.

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Ward, Sarah M., Diana S. Himmelstein, Jody K. Lancia, and Lester I. Binder. "Tau oligomers and tau toxicity in neurodegenerative disease." Biochemical Society Transactions 40, no. 4 (July 20, 2012): 667–71. http://dx.doi.org/10.1042/bst20120134.

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AD (Alzheimer's disease) is a progressive neurodegenerative disorder characterized by the extracellular accumulation of amyloid β-peptide and the intracellular accumulation of tau. Although there is much evidence linking tau to neurodegeneration, the precise mechanism of tau-mediated neurotoxicity remains elusive. The presence of tau-positive pre-tangle neurons lacking neurofibrillary tangles has been reported in AD brain tissue. In order to study this non-fibrillar tau, we generated a novel monoclonal antibody, named TOC1 (tau oligomeric complex 1), which selectively labels tau dimers and oligomers, but does not label filaments. Time-course analysis and antibody labelling indicates that oligomers appear as an early event in AD pathogenesis. Using a squid axoplasm assay, we have demonstrated that aggregated tau inhibits anterograde FAT (fast axonal transport), whereas monomeric tau has no effect. This inhibition requires a small stretch of N-terminal amino acids termed the PAD (phosphatase-activation domain). Using a PAD-specific antibody, TNT1 (tau N-terminal 1), we demonstrate that PAD exposure is increased in diseased neurons and this leads to an increase in FAT inhibition. Antibody co-labelling with the early-AD marker AT8 indicates that, similar to TOC1, TNT1 expression represents an early event in AD pathogenesis. Finally, the effects of the molecular chaperone Hsp70 (heat-shock protein 70) were also investigated within the squid axoplasm assay. We illustrate that Hsp70 preferentially binds to tau oligomers over filaments and prevents anterograde FAT inhibition observed with a mixture of both forms of aggregated tau. Together, these findings support the hypothesis that tau oligomers are the toxic form of tau in neurodegenerative disease.

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Khan, Md Ishak, Kathleen Gilpin, Fuad Hasan, Khandakar Abu Hasan Al Mahmud, and Ashfaq Adnan. "Effect of Strain Rate on Single Tau, Dimerized Tau and Tau-Microtubule Interface: A Molecular Dynamics Simulation Study." Biomolecules 11, no. 9 (September 4, 2021): 1308. http://dx.doi.org/10.3390/biom11091308.

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Microtubule-associated protein (MAP) tau is a cross-linking molecule that provides structural stability to axonal microtubules (MT). It is considered a potential biomarker for Alzheimer’s disease (AD), dementia, and other neurological disorders. It is also a signature protein for Traumatic Brain Injury (TBI) assessment. In the case of TBI, extreme dynamic mechanical energies can be felt by the axonal cytoskeletal members. As such, fundamental understandings of the responses of single tau protein, polymerized tau protein, and tau-microtubule interfaces under high-rate mechanical forces are important. This study attempts to determine the high-strain rate mechanical behavior of single tau, dimerized tau, and tau-MT interface using molecular dynamics (MD) simulation. The results show that a single tau protein is a highly stretchable soft polymer. During deformation, first, it significantly unfolds against van der Waals and electrostatic bonds. Then it stretches against strong covalent bonds. We found that tau acts as a viscoelastic material, and its stiffness increases with the strain rate. The unfolding stiffness can be ~50–500 MPa, while pure stretching stiffness can be >2 GPa. The dimerized tau model exhibits similar behavior under similar strain rates, and tau sliding from another tau is not observed until it is stretched to >7 times of original length, depending on the strain rate. The tau-MT interface simulations show that very high strain and strain rates are required to separate tau from MT suggesting Tau-MT bonding is stronger than MT subunit bonding between themselves. The dimerized tau-MT interface simulations suggest that tau-tau bonding is stronger than tau-MT bonding. In summary, this study focuses on the structural response of individual cytoskeletal components, namely microtubule (MT) and tau protein. Furthermore, we consider not only the individual response of a component, but also their interaction with each other (such as tau with tau or tau with MT). This study will eventually pave the way to build a bottom-up multiscale brain model and analyze TBI more comprehensively.

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Tchounwou, Christine, Bretton Fletcher, Chaeyeon Song, Phillip A. Kohl, Peter J. Chung, Herb P. Miller, Youli Li, et al. "The Effect of Site-Specific Acetylation Based Tau Mutations on Tau-Microtubule Associations." Biophysical Journal 116, no. 3 (February 2019): 255a. http://dx.doi.org/10.1016/j.bpj.2018.11.1391.

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He, Rong-Qiao, and Jian-Ying Luo. "Effect Of Acetaldehyde On Aggregation Of Neuronal Tau." Protein & Peptide Letters 6, no. 2 (April 1999): 105–10. http://dx.doi.org/10.2174/092986650602221108163847.

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Abstract: Acetaldehyde at a low concentration (0.25%) induces recombinant tau polymeriz.ation distinguishably without using chemic.al cross-linker disuccinimidyl su (DSS). The aggregation of the hyperphosphorylated tau occurs in the solution of acetaldehyde at 0.05%. It appears that formation of neurofibrillary tangles in alcoholics may be correlated to acetaldehyde besides alcoho and the abnormal tau phosphorylation may accelerate acetaldehyde-induced tau polymeriz.ation.

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Be, Rong-Qiao, Jian-Ying Luo, and Wei Li. "Effect of alcohol on aggregation of human neuronal tau protein." Protein & Peptide Letters 5, no. 5 (October 1998): 279–85. http://dx.doi.org/10.2174/092986650505221111094232.

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Abstract: Effects of alcohol and heparin on aggregation of the recombinant tau have been studied. Alcohol at low concentrations induces tau polymerization distinguishably at room temperature and 37°C. The effect of heparin on tau's aggregation was cooperative with that of alcohol if both heparin and alcohol were added to tau solutions. It appears that the polymerization of tau might be correlated to the disorder of neuronal transportation of alcoholism.

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Epremyan, Khoren K., Tatyana N. Goleva, and Renata A. Zvyagilskaya. "Effect of Tau Protein on Mitochondrial Functions." Biochemistry (Moscow) 87, no. 8 (August 2022): 689–701. http://dx.doi.org/10.1134/s0006297922080028.

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TSUJII, H. "Distributed $tau;2 effect in relaxation calorimetry." Physica B: Condensed Matter 329-333 (May 2003): 1552–53. http://dx.doi.org/10.1016/s0921-4526(02)02291-3.

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15

Boetger, C. L., and D. S. Ward. "Effect of dopamine on transient ventilatory response to exercise." Journal of Applied Physiology 61, no. 6 (December 1, 1986): 2102–7. http://dx.doi.org/10.1152/jappl.1986.61.6.2102.

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The effect of exogenous dopamine on the development of exercise hyperpnea was studied. Using a bicycle ergometer, five subjects performed repetitive square-wave work-load testing from unloaded pedaling to 80% of each subject's estimated anaerobic threshold. The breath-by-breath ventilation (VE), CO2 production (VCO2), and O2 consumption (VO2) responses were analyzed by curve fitting a first-order exponential model. Comparisons were made between control experiments and experiments with a 3-micrograms X kg-1 X min-1 intravenous infusion of dopamine. Steady-state VE, VCO2 and VO2 were unchanged by the dopamine infusion, both during unloaded pedaling and at the heavier work load. The time constants for the increase in VE (tau VE) and VCO2 (tau CO2) were significantly (P less than 0.05) slowed (tau VE = 56.5 +/- 16.4 s for control, and tau VE = 76.4 +/- 26.6 s for dopamine; tau CO2 = 51.5 +/- 10.6 s for control, and tau CO2 = 64.8 +/- 17.4 s for dopamine) (mean +/- SD), but the time constant for VO2 (tau O2) was not significantly affected (tau O2 = 27.5 +/- 11.7 s for control, and tau O2 = 31.0 +/- 10.1 s for dopamine). We conclude that ablation of carotid body chemosensitivity with dopamine slows the transient ventilatory response to exercise while leaving the steady-state response unaffected.

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Shin, Soo Jung, Yong Ho Park, Seong Gak Jeon, Sujin Kim, Yunkwon Nam, Sang-Muk Oh, Yong Yook Lee, and Minho Moon. "Red Ginseng Inhibits Tau Aggregation and Promotes Tau Dissociation In Vitro." Oxidative Medicine and Cellular Longevity 2020 (July 1, 2020): 1–12. http://dx.doi.org/10.1155/2020/7829842.

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Tau, a microtubule-associated protein expressed in mature neurons, interacts with tubulin to promote the assembly and stabilization of microtubules. However, abnormally hyperphosphorylated tau dissociates from microtubules and self-aggregates. Tau aggregates, including paired helical filaments and neurofibrillary tangles, promote neuronal dysfunction and death and are the defining neuropathological feature of tauopathies. Therefore, suppressing tau aggregation or stimulating the dissociation of tau aggregates has been proposed as an effective strategy for treating neurodegenerative diseases associated with tau pathology such as Alzheimer’s disease (AD) and frontotemporal dementia. Interestingly, ginsenosides extracted from Panax ginseng reduced the hippocampal and cortical expression of phosphorylated tau in a rat model of AD. However, no studies have been conducted into the effect of red ginseng (RG) and its components on tau pathology. Here, we evaluated the effect of Korean red ginseng extract (KRGE) and its components on the aggregation and disassociation of tau. Using the thioflavin T assay, we monitored the change in fluorescence produced by the aggregation or disassociation of tau K18, an aggregation-prone fragment of tau441 containing the microtubule-binding domain. Our analysis revealed that KRGE not only inhibited tau aggregation but also promoted the dissociation of tau aggregates. In addition, the KRGE fractions, such as saponin, nonsaponin, and nonsaponin fraction with rich polysaccharide, also inhibited tau aggregation and promoted the dissociation of tau aggregates. Our observations suggest that RG could be a potential therapeutic agent for the treatment of neurodegenerative diseases associated with tauopathy.

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Veselkina, Ekaterina R., Mikhail V. Trostnikov, Natalia V. Roshina, and Elena G. Pasyukova. "The Effect of the Tau Protein on D. melanogaster Lifespan Depends on GSK3 Expression and Sex." International Journal of Molecular Sciences 24, no. 3 (January 21, 2023): 2166. http://dx.doi.org/10.3390/ijms24032166.

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The microtubule-associated conserved protein tau has attracted significant attention because of its essential role in the formation of pathological changes in the nervous system, which can reduce longevity. The study of the effects caused by tau dysfunction and the molecular mechanisms underlying them is complicated because different forms of tau exist in humans and model organisms, and the changes in protein expression can be multidirectional. In this article, we show that an increase in the expression of the main isoform of the Drosophila melanogaster tau protein in the nervous system has differing effects on lifespan depending on the sex of individuals but has no effect on the properties of the nervous system, in particular, the synaptic activity and distribution of another microtubule-associated protein, Futsch, in neuromuscular junctions. Reduced expression of tau in the nervous system does not affect the lifespan of wild-type flies, but it does increase the lifespan dramatically shortened by overexpression of the shaggy gene encoding the GSK3 (Glycogen Synthase Kinase 3) protein kinase, which is one of the key regulators of tau phosphorylation levels. This effect is accompanied by the normalization of the Futsch protein distribution impaired by shaggy overexpression. The results presented in this article demonstrate that multidirectional changes in tau expression can lead to effects that depend on the sex of individuals and the expression level of GSK3.

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Klingbeil, David A., Ethan R. Van Norman, Katherine E. McLendon, Sarah G. Ross, and John C. Begeny. "Evaluating Tau-U With Oral Reading Fluency Data and the Impact of Measurement Error." Behavior Modification 43, no. 3 (March 12, 2018): 413–38. http://dx.doi.org/10.1177/0145445518760174.

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Recently, researchers have argued that using quantitative effect sizes in single-case design (SCD) research may facilitate the identification evidence-based practices. Indices to quantify nonoverlap are among the most common methods for quantifying treatment effects in SCD research. Tau-U represents a family of effect size indices that were developed to address criticisms of previously developed measures of nonoverlap. However, more research is necessary to determine the extent to which Tau-U successfully addresses proposed limitations of other nonoverlap methods. This study evaluated Tau-U effect sizes, derived from multiple-baseline designs, where researchers used curriculum-based measures of reading (CBM-R) to measure reading fluency. Specifically, we evaluated the distribution of the summary Tau-U statistic when applied to a large set of CBM-R data and assessed how the variability inherent in CBM-R data may influence the obtained Tau-U values. Findings suggest that the summary Tau-U statistic may be susceptible to ceiling effects. Moreover, the results provide initial evidence that error inherent in CBM-R scores may have a small but meaningful influence on the obtained effect sizes. Implications and recommendations for research and practice are discussed.

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DeTure, Michael, Li-wen Ko, Samuel Yen, Parimala Nacharaju, Colin Easson, Jada Lewis, Marjon van Slegtenhorst, Michael Hutton, and Shu-Hui Yen. "Missense tau mutations identified in FTDP-17 have a small effect on tau–microtubule interactions." Brain Research 853, no. 1 (January 2000): 5–14. http://dx.doi.org/10.1016/s0006-8993(99)02124-1.

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Kuznetsov, I. A., and A. V. Kuznetsov. "Simulating the effect of formation of amyloid plaques on aggregation of tau protein." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 474, no. 2220 (December 2018): 20180511. http://dx.doi.org/10.1098/rspa.2018.0511.

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In this paper, we develop a mathematical model that enables the investigation of the production and intracellular transport of amyloid precursor protein (APP) and tau protein in a neuron. We also investigate the aggregation of APP fragments into amyloid-β (Aβ) as well as tau aggregation into tau oligomers and neurofibrillary tangles. Using the developed model, we investigate how Aβ aggregation can influence tau transport and aggregation in both the soma and the axon. We couple the Aβ and tau agglomeration processes by assuming that the value of the kinetic constant that describes the autocatalytic growth (self-replication) reaction step of tau aggregation is proportional to the Aβ concentration. The model predicts that APP and tau are distributed differently in the axon. While APP has a uniform distribution along the axon, tau's concentration first decreases and then increases towards the synapse. Aβ is uniformly produced along the axon while misfolded tau protein is mostly produced in the proximal axon. The number of Aβ and tau polymers originating from the axon is much smaller than the number of Aβ and tau polymers originating from the soma. The rate of production of misfolded tau polymers depends on how strongly their production is facilitated by Aβ.

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Steen Jensen, Camilla, Erik Portelius, Volkert Siersma, Peter Høgh, Lene Wermuth, Kaj Blennow, Henrik Zetterberg, Gunhild Waldemar, Steen Gregers Hasselbalch, and Anja Hviid Simonsen. "Cerebrospinal Fluid Amyloid Beta and Tau Concentrations Are Not Modulated by 16 Weeks of Moderate- to High-Intensity Physical Exercise in Patients with Alzheimer Disease." Dementia and Geriatric Cognitive Disorders 42, no. 3-4 (2016): 146–58. http://dx.doi.org/10.1159/000449408.

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Background: Physical exercise may have some effect on cognition in patients with Alzheimer disease (AD). However, the underlying biochemical effects are unclear. Animal studies have shown that amyloid beta (Aβ), one of the pathological hallmarks of AD, can be altered with high levels of physical activity. Aim: The objective of this study was to elucidate the effect of 16 weeks of moderate- to high-intensity physical exercise on the biomarkers of AD, with special emphasis on the amyloidogenic pathway. Methods: From a total of 53 patients with AD participating in the Preserving Cognition, Quality of Life, Physical Health and Functional Ability in Alzheimer's Disease: The Effect of Physical Exercise (ADEX) study we analyzed cerebrospinal fluid samples for Aβ species, total tau (t-tau), phosphorylated tau (p-tau) and soluble amyloid precursor protein (sAPP) species. We also assessed the patients for apolipoprotein E ε4 (ApoE ε4) genotype. Results: We found no effect of 16 weeks of physical exercise on the selected biomarkers, and no effect of ApoE ε4 genotype. Conclusion: Our findings suggest that the possible effect of physical exercise on cognition in patients with AD is not due to modulation of Aβ, t-tau, p-tau and sAPP species.

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Feizabadi, Mitra Shojania, and Venise Jan Castillon. "The Effect of Tau and Taxol on Polymerization of MCF7 Microtubules In Vitro." International Journal of Molecular Sciences 23, no. 2 (January 8, 2022): 677. http://dx.doi.org/10.3390/ijms23020677.

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Overexpression of Tau protein in breast cancer cells is identified as an indicator for potential resistance to taxane-based therapy. As reported findings have been obtained mostly from clinical studies, the undetermined underlying mechanism of such drug resistance needs to be thoroughly explored through comprehensive in vitro evaluations. Tau and Taxol bind to the beta tubulin site in microtubules’ structure. This is of particular interest in breast cancer, as microtubules of these cancer cells are structurally distinct from some other microtubules, such as neuronal microtubules, due to their unique beta tubulin isotype distribution. The observed changes in the in vitro polymerization of breast cancer microtubules, and the different function of some molecular motors along them, leave open the possibility that the drug resistance mechanism can potentially be associated with different responses of these microtubules to Tau and Taxol. We carried out a series of parallel experiments to allow comparison of the in vitro dual effect of Tau and Taxol on the polymerization of MCF7 microtubules. We observed a concentration-dependent demotion-like alteration in the self-polymerization kinetics of Tau-induced MCF7 microtubules. In contrast, microtubules polymerized under the simultaneous effects of Tau and Taxol showed promoted assembly as compared with those observed in Tau-induced microtubules. The analysis of our data obtained from the length of MCF7 microtubules polymerized under the interaction with Tau and Taxol in vitro suggests that the phenomenon known as drug resistance in microtubule-targeted drugs such as Taxol may not be directly linked to the different responses of microtubules to the drug. The effect of the drug may be mitigated due to the simultaneous interactions with other microtubule-associated proteins such as Tau protein. The observed regulatory effect of Tau and Taxol on the polymerization of breast cancer microtubules in vitro points to additional evidence for the possible role of tubulin isotypes in microtubules’ functions.

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JONES, J., I. MOCIOIU, I. SARCEVIC, and M. H. RENO. "ULTRAHIGH ENERGY TAU NEUTRINOS." International Journal of Modern Physics A 20, no. 19 (July 30, 2005): 4656–63. http://dx.doi.org/10.1142/s0217751x0502834x.

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We study ultrahigh energy astrophysical neutrinos and the contribution of tau neutrinos from neutrino oscillations, relative to the contribution of the other flavors. We show the effect of tau neutrino regeneration and tau energy loss as they propagate through the Earth. We consider a variety of neutrino fluxes, such as cosmogenic neutrinos and neutrinos that originate in Active Galactic Nuclei. We discuss signals of tau neutrinos in detectors such as IceCube, RICE and ANITA.

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Spydell, Matthew S., and Falk Feddersen. "The effect of a non-zero Lagrangian time scale on bounded shear dispersion." Journal of Fluid Mechanics 691 (December 13, 2011): 69–94. http://dx.doi.org/10.1017/jfm.2011.443.

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AbstractPrevious studies of shear dispersion in bounded velocity fields have assumed random velocities with zero Lagrangian time scale (i.e. velocities are$\delta $-function correlated in time). However, many turbulent (geophysical and engineering) flows with mean velocity shear exist where the Lagrangian time scale is non-zero. Here, the longitudinal (along-flow) shear-induced diffusivity in a two-dimensional bounded velocity field is derived for random velocities with non-zero Lagrangian time scale${\tau }_{L} $. A non-zero${\tau }_{L} $results in two-time transverse (across-flow) displacements that are correlated even for large (relative to the diffusive time scale${\tau }_{D} $) times. The longitudinal (along-flow) shear-induced diffusivity${D}_{S} $is derived, accurate for all${\tau }_{L} $, using a Lagrangian method where the velocity field is periodically extended to infinity so that unbounded transverse particle spreading statistics can be used to determine${D}_{S} $. The non-dimensionalized${D}_{S} $depends on time and two parameters: the ratio of Lagrangian to diffusive time scales${\tau }_{L} / {\tau }_{D} $and the release location. Using a parabolic velocity profile, these dependencies are explored numerically and through asymptotic analysis. The large-time${D}_{S} $is enhanced relative to the classic Taylor diffusivity, and this enhancement increases with$ \sqrt{{\tau }_{L} } $. At moderate${\tau }_{L} / {\tau }_{D} = 0. 1$this enhancement is approximately a factor of 3. For classic shear dispersion with${\tau }_{L} = 0$, the diffusive time scale${\tau }_{D} $determines the time dependence and large-time limit of the shear-induced diffusivity. In contrast, for sufficiently large${\tau }_{L} $, a shear time scale${\tau }_{S} = \mathop{ ({\tau }_{L} {\tau }_{D} )}\nolimits ^{1/ 2} $, anticipated by a simple analysis of the particle’s domain-crossing time, determines both the${D}_{S} $time dependence and the large-time limit. In addition, the scalings for turbulent shear dispersion are recovered from the large-time${D}_{S} $using properties of wall-bounded turbulence.

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Sadot, E., J. Barg, D. Rasouly, P. Lazarovici, and I. Ginzburg. "Short- and long-term mechanisms of tau regulation in PC12 cells." Journal of Cell Science 108, no. 8 (August 1, 1995): 2857–64. http://dx.doi.org/10.1242/jcs.108.8.2857.

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Induction by nerve growth factor of neurite outgrowth in PC12 cells is transcription-dependent and is associated with the accumulation of tau protein. It was recently shown that short-term treatment with staurosporine, a protein kinase alkaloid inhibitor, induced an elevation of tau protein levels and outgrowth of stable neurites. In this study, we analyzed the mechanism(s) by which nerve growth factor and staurosporine exert their effects on tau levels. We demonstrate that nerve growth factor affects tau mRNA stability, thus contributing to the observed increase in tau mRNA levels. On the other hand, tau mRNA levels were not affected by the treatment with staurosporine. We also demonstrate that the phosphorylation of tau protein was reduced after treatment of PC12 cells with nerve growth factor or staurosporine, as shown by immunoblot analysis using specific antibodies and alkaline phosphatase treatment. Thus, regulation of tau levels by nerve growth factor appears to be mediated by transcriptional, post-transcriptional and posttranslational steps, whereas the effect of staurosporine on tau levels may be attributed to its effect on the state of phosphorylation of the protein.

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Niewiadomska, Grazyna, Wiktor Niewiadomski, Marta Steczkowska, and Anna Gasiorowska. "Tau Oligomers Neurotoxicity." Life 11, no. 1 (January 6, 2021): 28. http://dx.doi.org/10.3390/life11010028.

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Although the mechanisms of toxic activity of tau are not fully recognized, it is supposed that the tau toxicity is related rather not to insoluble tau aggregates but to its intermediate forms. It seems that neurofibrillar tangles (NFTs) themselves, despite being composed of toxic tau, are probably neither necessary nor sufficient for tau-induced neuronal dysfunction and toxicity. Tau oligomers (TauOs) formed during the early stages of tau aggregation are the pathological forms that play a key role in eliciting the loss of neurons and behavioral impairments in several neurodegenerative disorders called tauopathies. They can be found in tauopathic diseases, the most common of which is Alzheimer’s disease (AD). Evidence of co-occurrence of b-amyloid, α-synuclein, and tau into their most toxic forms, i.e., oligomers, suggests that these species interact and influence each other’s aggregation in several tauopathies. The mechanism responsible for oligomeric tau neurotoxicity is a subject of intensive investigation. In this review, we summarize the most recent literature on the damaging effect of TauOs on the stability of the genome and the function of the nucleus, energy production and mitochondrial function, cell signaling and synaptic plasticity, the microtubule assembly, neuronal cytoskeleton and axonal transport, and the effectiveness of the protein degradation system.

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Neitzel, Julia, Nicolai Franzmeier, Anna Rubinski, and Michael Ewers. "Left frontal connectivity attenuates the adverse effect of entorhinal tau pathology on memory." Neurology 93, no. 4 (June 24, 2019): e347-e357. http://dx.doi.org/10.1212/wnl.0000000000007822.

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ObjectiveTo investigate whether higher global left frontal cortex (gLFC) connectivity, a putative neural substrate of cognitive reserve, attenuates the effect of entorhinal tau PET levels on episodic memory in older adults.MethodsCross-sectional 18F-AV-1451 PET (to assess tau pathology), 18F-AV-45 or 18F-BAY94-9172 PET (to assess β-amyloid [Aβ]), and resting-state fMRI were obtained in 125 elderly participants from the Alzheimer's Neuroimaging Initiative, including 82 cognitively normal participants (amyloid PET-positive [Aβ+], n = 27) and 43 patients with amnestic mild cognitive impairment (Aβ+ = 15). Resting-state fMRI gLFC connectivity was computed for each participant as the average functional connectivity between the left frontal cortex (LFC) (seed) and each remaining voxel in the gray matter. As a measure of tau pathology, we assessed the mean tau PET uptake in the entorhinal cortex. In linear mixed-effects regression analysis, we tested the interaction term gLFC connectivity × entorhinal tau PET on delayed free recall performance. In addition, we assessed whether higher connectivity of the whole frontoparietal control network (FPCN), of which the LFC is a major hub, is associated with reserve.ResultsHigher entorhinal tau PET was strongly associated with poorer delayed free recall performance (β/SE = −0.49/0.07, p < 0.001). A significant gLFC connectivity × entorhinal tau PET interaction was found (β/SE = 0.19/0.06, p = 0.003), such that at higher levels of gLFC connectivity, the decrease in memory score per unit of entorhinal tau PET was attenuated. The FPCN connectivity × tau interaction was also significant (β/SE = 0.10/0.04, p = 0.012).ConclusionBoth gLFC and FPCN connectivity are associated with higher resilience against the adverse effect of early-stage entorhinal tau pathology on memory performance.

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Berrocal, Maria, Montaña Caballero-Bermejo, Carlos Gutierrez-Merino, and Ana M. Mata. "Methylene Blue Blocks and Reverses the Inhibitory Effect of Tau on PMCA Function." International Journal of Molecular Sciences 20, no. 14 (July 18, 2019): 3521. http://dx.doi.org/10.3390/ijms20143521.

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Methylene blue (MB) is a synthetic phenothiazine dye that, in the last years, has generated much debate about whether it could be a useful therapeutic drug for tau-related pathologies, such as Alzheimer’s disease (AD). However, the molecular mechanism of action is far from clear. Recently we reported that MB activates the plasma membrane Ca2+-ATPase (PMCA) in membranes from human and pig tissues and from cells cultures, and that it could protect against inactivation of PMCA by amyloid β-peptide (Aβ). The purpose of the present study is to further examine whether the MB could also modulate the inhibitory effect of tau, another key molecular marker of AD, on PMCA activity. By using kinetic assays in membranes from several tissues and cell cultures, we found that this phenothiazine was able to block and even to completely reverse the inhibitory effect of tau on PMCA. The results of this work point out that MB could mediate the toxic effect of tau related to the deregulation of calcium homeostasis by blocking the impairment of PMCA activity by tau. We then could conclude that MB could interfere with the toxic effects of tau by restoring the function of PMCA pump as a fine tuner of calcium homeostasis.

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Frédérick, Christelle, Karelle Leroy, and Jean-Pierre Brion. "O3-04-08: In vivo stimulation of macroautophagy: Effect on tau accumulation in neurons and on tau pathology in mutant tau mice." Alzheimer's & Dementia 7 (July 2011): S507. http://dx.doi.org/10.1016/j.jalz.2011.05.1414.

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Ceccotti, Chiara, Basim S. A. Al-Sulaivany, Omar A. M. Al-Habbib, Marco Saroglia, Simona Rimoldi, and Genciana Terova. "Protective Effect of Dietary Taurine from ROS Production in European Seabass under Conditions of Forced Swimming." Animals 9, no. 9 (August 26, 2019): 607. http://dx.doi.org/10.3390/ani9090607.

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Taurine (Tau) is an amino sulfonic acid, which is widely distributed in animal tissues, whereas it is almost lacking in plants with the exception of certain algae, seaweeds, and few others. In the aquafeed industry, Tau is mainly used as a feed additive to promote growth in marine fish species with limited cysteine sulfinate decarboxylase activity. In particular, Tau supplementation is required in feeds in which fishmeal (FM) is substituted with high percentages of plant-derived protein sources such as soybean meals (SBM) that have much lower levels of Tau than FM. In addition to being a growth promoter, Tau exert powerful antioxidant properties being a scavenger of the reactive oxygen species (ROS). Under sustained swimming conditions, an intracellular increase in ROS production can occur in fish red muscle where the abundance of mitochondria (the main site of ROS formation) is high. Accordingly, this study aimed at investigating the effects of dietary Tau on European seabass (Dicentrarchus labrax) growth and oxidative stress response induced by swimming exercise. Individually tagged fish of 92.57 ± 20.33 g mean initial weight were fed two experimental diets containing the same low percentage of FM and high percentage of SBM. One diet was supplemented with 1.5% of Tau. Tau supplemented in the diet had a positive effect on fish growth, and enhanced swimming performance and antioxidant status. Two swim endurance tests were performed during the feeding trial. Metabolic oxygen consumption (MO2) was measured during exercise at incremental swimming speeds (0.7, 1.4, 2.1, 2.8, 3.5, and then 4.2 BL (body length) s−1, until fatigue). Fish maximal sustainable swimming speed (Ucrit) was determined too. To investigate the antioxidant effect of dietary Tau, we also measured ROS production in fish blood by RBA (respiratory burst activity) assay and quantified the expression of genes coding for antioxidant enzymes by qPCR (quantitative polymerase chain reaction) , such as SOD (superoxide dismutase), GPX (glutathione peroxidase), and CAT (catalase) in red muscle and liver. There was a significant effect of Tau upon Ucrit during exercise. Additionally, ROS production was significantly lower in fish fed with Tau supplemented diet, supporting the role of Tau as ROS scavenger. The protective effect of Tau against oxidative stress induced by forced swimming was denoted also by a significant decrease in antioxidant enzymes gene expression in fish liver and muscle. Taken together these results demonstrate that Tau is beneficial in low FM-based diets for seabass.

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Ising, Christina, Gilbert Gallardo, Cheryl E. G. Leyns, Connie H. Wong, Hong Jiang, Floy Stewart, Lauren J. Koscal, et al. "AAV-mediated expression of anti-tau scFvs decreases tau accumulation in a mouse model of tauopathy." Journal of Experimental Medicine 214, no. 5 (April 17, 2017): 1227–38. http://dx.doi.org/10.1084/jem.20162125.

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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 HJ8.5 with variable linker lengths, all specific to human tau. Based on different binding properties, we selected two anti-tau scFvs and tested their efficacy in vivo by adeno-associated virus–mediated gene transfer to the brain of P301S-tg mice. The scFvs significantly reduced levels of hyperphosphorylated, aggregated tau in brain tissue of P301S-tg mice, associated with a decrease in detergent-soluble tau species. Interestingly, these mice showed substantial levels of scFvs in the cerebrospinal fluid without significant effects on total extracellular tau levels. Therefore, our study provides a novel strategy for anti-tau immunotherapeutics that potentially limits a detrimental proinflammatory response.

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Liu, Yunsheng, Lan Cao, Xiaoxu Zhang, Yan Liang, Yuxia Xu, and Cuiqing Zhu. "Memantine Differentially Regulates Tau Phosphorylation Induced by Chronic Restraint Stress of Varying Duration in Mice." Neural Plasticity 2019 (February 14, 2019): 1–18. http://dx.doi.org/10.1155/2019/4168472.

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Exposure to chronic psychiatric stress has been linked to Alzheimer’s disease-related tau hyperphosphorylation and abnormalities in glutamate neurotransmission. However, the pathological relationship between glutamatergic dysfunction and tau phosphorylation in the cerebral cortex under chronic psychiatric stress is not fully understood. The present study investigated the effects of memantine (MEM, 5 and 10 mg/kg), an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, on chronic restraint stress- (CRS-) induced tau phosphorylation in mice. CRS administered for 16 or 28 consecutive days (1 h daily) induced significant tau phosphorylation in the brain. MEM treatment suppressed the elevation of phosphorylated tau (P-tau) levels induced by 16-day CRS in a dose-dependent manner. P-tau reduction was accompanied by the attenuation of the upregulation of GSK3β and CDK5 expression and the downregulation of PP2A activity induced by CRS. Additionally, MEM reduced CRS-induced upregulation of NMDA receptor subunit levels (GluN2A, GluN2B) in the frontal cortex. However, MEM markedly enhanced tau phosphorylation in the frontal cortex and other cerebral cortical regions following 28 days of CRS. The stimulatory effect of MEM on CRS-induced tau phosphorylation was correlated with increased activities of AKT, JNK, and GSK3β, inactivation of PP2A, and downregulation of Pin1 and HSP70. Moreover, MEM did not effectively reverse the NMDA receptor upregulation induced by 28-day CRS and even increased GluN2B subunit levels. In contrast to the duration-dependent effects of MEM on P-tau levels, MEM produced an anxiolytic effect in both regimens as revealed by elevated plus maze testing. However, MEM did not affect the body weight reduction induced by CRS. Thus, MEM exerts distinctive effects on CRS-induced tau phosphorylation, which might be related to the expression of GluN2B. The differential effects of MEM on P-tau levels have crucial implications for its clinical application.

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Harris, Christopher J., Nora E. Gray, Maya Caruso, Marguex Hunter, Martina Ralle, and Joseph F. Quinn. "Copper Modulation and Memory Impairment due to Hippocampal Tau Pathology." Journal of Alzheimer's Disease 78, no. 1 (October 27, 2020): 49–60. http://dx.doi.org/10.3233/jad-200002.

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Background: Environmental copper has been implicated in the pathogenesis of Alzheimer’s disease based on evidence that: 1) brain copper levels increase with age, 2) copper promotes misfolding and toxicity of amyloid-β in vitro, 3) copper-modulating interventions reduce amyloid pathology in animal models. However, the effect of copper upon non-amyloid Alzheimer’s pathology is relatively under-explored. Objective: To determine if modulation of brain copper level affects brain tau pathology and/or associated cognitive impairment. Methods: We tested the hypothesis that brain copper modulates tau pathology by manipulating brain levels of copper in the PS19 transgenic mouse model of tau pathology. We treated PS19 and wild-type mice with oral zinc acetate, an established therapy for long term control of excess brain copper, and examined treatment effects upon brain copper, brain tau, NFT-like pathology, and spatial memory. We treated a second cohort of mice with exogenous dietary copper in order to evaluate whether excess environmental copper promotes brain tau pathology. Results: Copper-lowering with oral zinc attenuated spatial memory impairment in female but not male PS19 mice, without a significant effect upon tau pathology. Copper loading increased brain copper, but did not have an effect on brain tau pathology or spatial memory function. Conclusion: These findings suggest that a strategy to lower brain copper may be viable for symptomatic benefit in the setting of tau neuropathology, but unlikely to have robust effects on the underlying pathology. These findings are consistent with dietary or other exogenous copper being unlikely to promote tau pathology.

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MUSA, S. I., K. O. YAHAYA, and A. YAHAYA. "COMPUTATIONAL ANALYSIS OF FUNCTIONAL EFFECTS OF SINGLE NUCLEOTIDE POLYMORPHISM ON OVINE INTERFERON TAU." FUDMA Journal of Agriculture and Agricultural Technology 8, no. 1 (September 15, 2022): 26–29. http://dx.doi.org/10.33003/jaat.2022.0801.071.

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The objective of this study was to evaluate the functional effects of Single Nucleotide Polymorphism(SNP) in ovine interferon tau using computational methods. Data on ovine interferon was retrieved from data base of National Center for Biotechnology Information ((GenBank). Functional effects of substitution of Leucin by Proline at position 26 of interferon protein chain was predicted using Protein Variation Effect Analyser, Panther server and Poly phen 2 (Polymorphism phenotyping). Provean score of - 5.828 was obtained, indicating a deleterious effect of the amino acid substitution. Panther server indicated damaging effect of the SNP with Pdel ( probability of deleterious effect) of 0.5. Similarly, Poly phen 2 showed damaging effect of the amino acid substitution. It can be concluded that substitution of Leucin by proline at position 26 of the protein sequence of interferon tau resulted in deleterious effect on the functionality of ovine interferon tau. Studies in Single Nucleotide Polymorphism on ovine interferon tau can provide better understanding of biomarkers associated with efficiency of maternal pregnancy recognition in the ovine species.

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Webster, Jack M., April L. Darling, Taylor A. Sanders, Danielle M. Blazier, Yamile Vidal-Aguiar, David Beaulieu-Abdelahad, Drew G. Plemmons, et al. "Hsp22 with an N-Terminal Domain Truncation Mediates a Reduction in Tau Protein Levels." International Journal of Molecular Sciences 21, no. 15 (July 30, 2020): 5442. http://dx.doi.org/10.3390/ijms21155442.

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Misfolding, aggregation and accumulation of proteins are toxic elements in the progression of a broad range of neurodegenerative diseases. Molecular chaperones enable a cellular defense by reducing or compartmentalizing these insults. Small heat shock proteins (sHsps) engage proteins early in the process of misfolding and can facilitate their proper folding or refolding, sequestration, or clearance. Here, we evaluate the effects of the sHsp Hsp22, as well as a pseudophosphorylated mutant and an N-terminal domain deletion (NTDΔ) variant on tau aggregation in vitro and tau accumulation and aggregation in cultured cells. Hsp22 wild-type (WT) protein had a significant inhibitory effect on heparin-induced aggregation in vitro and the pseudophosphorylated mutant Hsp22 demonstrated a similar effect. When co-expressed in a cell culture model with tau, these Hsp22 constructs significantly reduced soluble tau protein levels when transfected at a high ratio relative to tau. However, the Hsp22 NTDΔ protein drastically reduced the soluble protein expression levels of both tau WT and tau P301L/S320F even at lower transfection ratios, which resulted in a correlative reduction of the triton-insoluble tau P301L/S320F aggregates.

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Gu, Jianlan, Wen Xu, Nana Jin, Longfei Li, Yan Zhou, Dandan Chu, Cheng-Xin Gong, Khalid Iqbal, and Fei Liu. "Truncation of Tau selectively facilitates its pathological activities." Journal of Biological Chemistry 295, no. 40 (July 31, 2020): 13812–28. http://dx.doi.org/10.1074/jbc.ra120.012587.

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Neurofibrillary tangles of abnormally hyperphosphorylated Tau are a hallmark of Alzheimer's disease (AD) and related tauopathies. Tau is truncated at multiple sites by various proteases in AD brain. Although many studies have reported the effect of truncation on the aggregation of Tau, these studies mostly employed highly artificial conditions, using heparin sulfate or arachidonic acid to induce aggregation. Here, we report for the first time the pathological activities of various truncations of Tau, including site-specific phosphorylation, self-aggregation, binding to hyperphosphorylated and oligomeric Tau isolated from AD brain tissue (AD O-Tau), and aggregation seeded by AD O-Tau. We found that deletion of the first 150 or 230 amino acids (aa) enhanced Tau's site-specific phosphorylation, self-aggregation, and binding to AD O-Tau and aggregation seeded by AD O-Tau, but deletion of the first 50 aa did not produce a significant effect. Deletion of the last 50 aa was found to modulate Tau's site-specific phosphorylation, promote its self-aggregation, and cause it to be captured by and aggregation seeded by AD O-Tau, whereas deletion of the last 20 aa had no such effects. Among the truncated Taus, Tau151–391 showed the highest pathological activities. AD O-Tau induced aggregation of Tau151–391in vitro and in cultured cells. These findings suggest that the first 150 aa and the last 50 aa protect Tau from pathological characteristics and that their deletions facilitate pathological activities. Thus, inhibition of Tau truncation may represent a potential therapeutic approach to suppress Tau pathology in AD and related tauopathies.

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Aquin, Joshua P., Leslie E. Roos, Jino Distasio, Laurence Y. Katz, Jimmy Bourque, James M. Bolton, Shay-Lee Bolton, et al. "Effect of Housing First on Suicidal Behaviour." Canadian Journal of Psychiatry 62, no. 7 (February 27, 2017): 473–81. http://dx.doi.org/10.1177/0706743717694836.

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Objective: This study attempted to determine if Housing First (HF) decreased suicidal ideation and attempts compared to treatment as usual (TAU) amongst homeless persons with mental disorders, a population with a demonstrably high risk of suicidal behaviour. Method: The At Home/Chez Soi project is an unblinded, randomised control trial conducted across 5 Canadian cities (Vancouver, Winnipeg, Toronto, Montreal, Moncton) from 2009 to 2013. Homeless adults with a diagnosed major mental health disorder were recruited through community agencies and randomised to HF ( n = 1265) and TAU ( n = 990). HF participants were provided with private housing units and received case management support services. TAU participants retained access to existing community supports. Past-month suicidal ideation was measured at baseline and 6, 12, 18, and 21/24 months. A history of suicide attempts was measured at baseline and the 21/24-month follow-up. Results: Compared to baseline, there was an overall trend of decreased past-month suicidal ideation (estimate = –.57, SE = .05, P < 0.001), with no effect of treatment group (i.e., HF vs. TAU; estimate = –.04, SE = .06, P = 0.51). Furthermore, there was no effect of treatment status (estimate = –.10, SE = .16, P = 0.52) on prevalence of suicide attempts (HF = 11.9%, TAU = 10.5%) during the 2-year follow-up period. Conclusion: This study failed to find evidence that HF is superior to TAU in reducing suicidal ideation and attempts. We suggest that HF interventions consider supplemental psychological treatments that have proven efficacy in reducing suicidal behaviour. It remains to be determined what kind of suicide prevention interventions (if any) are specifically effective in further reducing suicidal risk in a housing-first intervention.

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Paál, Dušan, František Strejček, Eva Tvrdá, Grzegorz Formicki, Sabine Klein, Detlef Rath, and Peter Massanyi. "The in Vitro Effect of Taurine on Boar Spermatozoa Quality." Acta Universitatis Agriculturae et Silviculturae Mendelianae Brunensis 66, no. 1 (2018): 131–37. http://dx.doi.org/10.11118/actaun201866010131.

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The aim of this in vitro study was to evaluate the effects of taurine (TAU) supplementation on boar spermatozoa motility, viability, acrosome integrity and morphology. Eighteen boar semen samples were diluted with the Androhep PlusTM extender containing no TAU (control) or supplemented with 1.5 mM, 7 mM, 12.5 mM TAU and cultured at 4 °C for 18 days. Sperm motility was evaluated using the computer-aided sperm analysis (CASA) system. Furthermore, the samples were fixed and assessed for the occurrence of morphological abnormalities using phase contrast microscopy. Fluorescent dyes SYBR – 14 and propidium iodide were used to determine the sperm viability. Acrosome integrity was examined using PNA – Alexa Fluor 647 and flow cytometry. A gradual decrease of the semen quality was detected in all experimental groups over the course of the study. CASA revealed no selective advantage of TAU supplementation on the spermatozoa motility (p > 0.05). TAU administration showed to be ineffective in preserving spermatozoa viability as well as acrosome integrity as measured by flow cytometry (p > 0.05). Under the conditions of this study, no significant positive effect of TAU was recorded following its administration to the Androhep PlusTM boar semen extender with respect to spermatozoa quality.

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Natale, Carmina, Maria Monica Barzago, Luca Colnaghi, Ada De Luigi, Franca Orsini, Luana Fioriti, and Luisa Diomede. "A Combined Cell-Worm Approach to Search for Compounds Counteracting the Toxicity of Tau Oligomers In Vivo." International Journal of Molecular Sciences 23, no. 19 (September 24, 2022): 11277. http://dx.doi.org/10.3390/ijms231911277.

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A clear relationship between the tau assemblies and toxicity has still to be established. To correlate the tau conformation with its proteotoxic effect in vivo, we developed an innovative cell-worm-based approach. HEK293 cells expressing tau P301L under a tetracycline-inducible system (HEK T-Rex) were employed to produce different tau assemblies whose proteotoxic potential was evaluated using C. elegans. Lysates from cells induced for five days significantly reduced the worm’s locomotor activity. This toxic effect was not related to the total amount of tau produced by cells or to its phosphorylation state but was related to the formation of multimeric tau assemblies, particularly tetrameric ones. We investigated the applicability of this approach for testing compounds acting against oligomeric tau toxicity, using doxycycline (Doxy) as a prototype drug. Doxy affected tau solubility and promoted the disassembly of already formed toxic aggregates in lysates of cells induced for five days. These effects translated into a dose-dependent protective action in C. elegans. These findings confirm the validity of the combined HEK T-Rex cells and the C. elegans-based approach as a platform for pharmacological screening.

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Tarlow, Kevin R. "An Improved Rank Correlation Effect Size Statistic for Single-Case Designs: Baseline Corrected Tau." Behavior Modification 41, no. 4 (November 9, 2016): 427–67. http://dx.doi.org/10.1177/0145445516676750.

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Measuring treatment effects when an individual’s pretreatment performance is improving poses a challenge for single-case experimental designs. It may be difficult to determine whether improvement is due to the treatment or due to the preexisting baseline trend. Tau- U is a popular single-case effect size statistic that purports to control for baseline trend. However, despite its strengths, Tau- U has substantial limitations: Its values are inflated and not bound between −1 and +1, it cannot be visually graphed, and its relatively weak method of trend control leads to unacceptable levels of Type I error wherein ineffective treatments appear effective. An improved effect size statistic based on rank correlation and robust regression, Baseline Corrected Tau, is proposed and field-tested with both published and simulated single-case time series. A web-based calculator for Baseline Corrected Tau is also introduced for use by single-case investigators.

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CHEN, Yong-Hui, Rong-Qiao HE, Ying LIU, Yang LIU, and Zhi-Gang XUE. "Effect of human neuronal tau on denaturation and reactivation of rabbit muscle D-glyceraldehyde-3-phosphate dehydrogenase." Biochemical Journal 351, no. 1 (September 26, 2000): 233–40. http://dx.doi.org/10.1042/bj3510233.

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Human neuronal tau-40 (htau-40) has been used to study denaturation and renaturation of rabbit muscle D-glyceraldehyde-3-phosphate dehydrogenase (GAPDH, EC 1.2.1.12). Inactivation of GAPDH incubated with tau was more distinguishably detected than that of control GAPDH during thermal and guanidine hydrochloride (GdnHCl) denaturation. However, tau did not influence the activity of GAPDH at room temperature or in solution without GdnHCl. A marked change in both the emission intensity and emission maximum of the intrinsic fluorescence at 335nm of GAPDH with tau was observed when GdnHCl concentration was 0.8M, but that of the control without tau occurred in 1.2M GdnHCl. The first-order rate of the decrease in the fluorescence intensity of the enzyme with tau was approximately twice as great as that of GAPDH without tau. Kinetics of inactivation of GAPDH with tau in 0.2M GdnHCl was a monophasic procedure, instead of the biphasic procedure followed by the control, as described before [He, Zhao, Yan and Li (1993) Biochim. Biophys. Acta 1163, 315–320]. Similar results were obtained when the enzyme was thermally denatured at 45°C. It revealed that tau bound to the denatured GAPDH but not the native molecule. On the other hand, tau suppressed refolding and reactivation of GAPDH when this enzyme was reactivated by dilution of GdnHCl solution. Furthermore, tau improved the aggregation of the non-native GAPDH in solutions. It suggested that tau acted in an anti-chaperone-like manner towards GAPDH in vitro. However, tau lost that function when it was aggregated or phosphorylated by neuronal cdc2-like protein kinase. It showed that tau's anti-chaperone-like function depended on its native conformation.

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Pontzer, C. H., J. K. Yamamoto, F. W. Bazer, T. L. Ott, and H. M. Johnson. "Potent anti-feline immunodeficiency virus and anti-human immunodeficiency virus effect of IFN-tau." Journal of Immunology 158, no. 9 (May 1, 1997): 4351–57. http://dx.doi.org/10.4049/jimmunol.158.9.4351.

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Abstract Ovine IFN-tau is a newly described protein related to IFN-alpha that is responsible for maternal recognition of pregnancy in sheep. It has been shown to exhibit potent antiviral and antiproliferative activity. To determine its antiviral activity against feline immunodeficiency virus (FIV) and HIV, the activity of the RNA-dependent DNA polymerase, reverse transcriptase, was assayed in FIV- and HIV-infected feline and human PBL treated with IFN-tau. Significant dose-dependent inhibition of reverse transcriptase activity by IFN-tau was detected by day 6 of culture and was maintained through the peak of virus replication. In addition, production of the FIV core protein, p25, was blocked by IFN-tau. Both the amino- and carboxyl-terminal regions of IFN-tau, as identified by synthetic peptides, appear to be involved in its antiretroviral activity. Comparison of the anti-HIV activities of IFN-tau and recombinant human IFN-alpha2 (rHuIFN-alpha2) indicated that while rHuIFN-alpha2 was toxic to cells at 10,000 U/ml, IFN-tau antiretroviral activity was not associated with a decrease in either cell viability or immunologic reactivity. Thus, IFN-tau displayed potent anti-FIV and anti-HIV activity without the cytotoxicity associated with high concentrations of rHuIFN-alpha2.

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Brandenburg, A., and K. Subramanian. "Minimal tau approximation and simulations of the alpha effect." Astronomy & Astrophysics 439, no. 3 (August 12, 2005): 835–43. http://dx.doi.org/10.1051/0004-6361:20053221.

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Li, Xia-Chun, Ze-Fen Wang, Jun-Xia Zhang, Qun Wang, and Jian-Zhi Wang. "Effect of melatonin on calyculin A-induced tau hyperphosphorylation." European Journal of Pharmacology 510, no. 1-2 (March 2005): 25–30. http://dx.doi.org/10.1016/j.ejphar.2005.01.023.

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Jho, Y. S., E. B. Zhulina, M. W. Kim, and P. A. Pincus. "Monte Carlo Simulations of Tau Proteins: Effect of Phosphorylation." Biophysical Journal 99, no. 8 (October 2010): 2387–97. http://dx.doi.org/10.1016/j.bpj.2010.06.056.

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Tanikawa, Nao, Yugo Suzue, Schuichi Matsuyama, Koji Kimura, Hisataka Iwata, Takehito Kuwayama, and Koumei Shirasuna. "The effect of interferon tau on human placental cells." Journal of Reproductive Immunology 118 (November 2016): 134. http://dx.doi.org/10.1016/j.jri.2016.10.075.

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Ismail, Tania, and Mathumai Kanapathipillai. "Effect of cellular polyanion mimetics on tau peptide aggregation." Journal of Peptide Science 24, no. 11 (September 24, 2018): e3125. http://dx.doi.org/10.1002/psc.3125.

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Rubio, Alicia, Mar Pérez, Luis de Lecea, and Jesús Ávila. "Effect of cortistatin on tau phosphorylation at Ser262 site." Journal of Neuroscience Research 86, no. 11 (August 15, 2008): 2462–75. http://dx.doi.org/10.1002/jnr.21689.

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Gauthier-Kemper, Anne, Carina Weissmann, Nataliya Golovyashkina, Zsofia Sebö-Lemke, Gerard Drewes, Volker Gerke, Jürgen J. Heinisch, and Roland Brandt. "The frontotemporal dementia mutation R406W blocks tau’s interaction with the membrane in an annexin A2–dependent manner." Journal of Cell Biology 192, no. 4 (February 21, 2011): 647–61. http://dx.doi.org/10.1083/jcb.201007161.

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Changes of the microtubule-associated protein tau are central in Alzheimer’s disease (AD) and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17). However, the functional consequence of the FTDP-17 tau mutation R406W, which causes a tauopathy clinically resembling AD, is not well understood. We find that the R406W mutation does not affect microtubule interaction but abolishes tau’s membrane binding. Loss of binding is associated with decreased trapping at the tip of neurites and increased length fluctuations during process growth. Tandem affinity purification tag purification and mass spectrometry identify the calcium-regulated plasma membrane–binding protein annexin A2 (AnxA2) as a potential interaction partner of tau. Consistently, wild-type tau but not R406W tau interacts with AnxA2 in a heterologous yeast expression system. Sequestration of Ca2+ or knockdown of AnxA2 abolishes the differential trapping of wild-type and R406W tau. We suggest that the pathological effect of the R406W mutation is caused by impaired membrane binding, which involves a functional interaction with AnxA2 as a membrane–cytoskeleton linker.

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Martini-Stoica, Heidi, Allysa L. Cole, Daniel B. Swartzlander, Fading Chen, Ying-Wooi Wan, Lakshya Bajaj, David A. Bader, et al. "TFEB enhances astroglial uptake of extracellular tau species and reduces tau spreading." Journal of Experimental Medicine 215, no. 9 (August 14, 2018): 2355–77. http://dx.doi.org/10.1084/jem.20172158.

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The progression of tau pathology in Alzheimer’s disease follows a stereotyped pattern, and recent evidence suggests a role of synaptic connections in this process. Astrocytes are well positioned at the neuronal synapse to capture and degrade extracellular tau as it transits the synapse and hence could potentially have the ability to inhibit tau spreading and delay disease progression. Our study shows increased expression and activity of Transcription Factor EB (TFEB), a master regulator of lysosomal biogenesis, in response to tau pathology in both human brains with dementia and transgenic mouse models. Exogenous TFEB expression in primary astrocytes enhances tau fibril uptake and lysosomal activity, while TFEB knockout has the reverse effect. In vivo, induced TFEB expression in astrocytes reduces pathology in the hippocampus of PS19 tauopathy mice, as well as prominently attenuates tau spreading from the ipsilateral to the contralateral hippocampus in a mouse model of tau spreading. Our study suggests that astrocytic TFEB plays a functional role in modulating extracellular tau and the propagation of neuronal tau pathology in tauopathies such as Alzheimer’s disease.

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Journal articles on the topic 'Tau Effect'

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