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Disease relevance of Tauopathies


Psychiatry related information on Tauopathies


High impact information on Tauopathies

  • However, neurodegeneration occurred without the neurofibrillary tangle formation that is seen in human disease and some rodent tauopathy models [7].
  • Thus, the ability of tau and alpha-synuclein to affect each other directly or indirectly might contribute to the overlap in the clinical and pathological features of tauopathies and synucleinopathies [8].
  • Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo [9].
  • These results reveal a mechanism of regulation of tau phosphorylation and suggest that abnormal hyperphosphorylation of tau could result from decreased tau O-GlcNAcylation, which probably is induced by deficient brain glucose uptake/metabolism in AD and other tauopathies [10].
  • Hsp70/CHIP may therefore play an important role in the pathogenesis of tauopathies and also represents a potential therapeutic target [11].

Chemical compound and disease context of Tauopathies

  • By directly comparing modifiers isolated in the models of polyglutamine diseases and in a Drosophila model of tauopathy, we find a final common pathway of cell death involving apoptosis [12].
  • Region-specific Dissociation of Neuronal Loss and Neurofibrillary Pathology in a Mouse Model of Tauopathy [13].
  • Identification of small molecule inhibitors of heparin-induced assembly of tau will form a starting point for the development of mechanism-based therapies for the tauopathies [14].
  • Administration of the female sex steroid and potent neuroprotective agent, 17beta-estradiol, reduced ischemia-reperfusion-induced cerebral damage and the subsequent aberrant mitosis and tauopathies [15].
  • Sarkosyl-insoluble tau exhibited 2 major bands of 64 and 68 kDa and a minor 72 kDa band, similar to the pattern seen in a familial tauopathy associated with an intronic tau mutation [16].

Biological context of Tauopathies


Anatomical context of Tauopathies


Gene context of Tauopathies

  • We conclude that although the cellular origin of ApoE4 differentially affects regional amyloid pathology, ApoE4 acts on the disposition of amyloid peptides downstream from their excision from APP but without induction of tauopathy [25].
  • In NPC1, early-onset tauopathy is a constant feature [26].
  • We examined the immunoreactivity of ubiquitin-binding protein p62 and its association with ubiquitin (Ub), alpha-synuclein, and paired helical filament (PHF)-tau in the affected brain areas of human tauopathies and synucleinopathies [27].
  • Ubiquitin-binding protein p62 is present in neuronal and glial inclusions in human tauopathies and synucleinopathies [27].
  • These findings indicate that MAPK/ERK-P, SAPK/JNK-P and p-38-P are differentially expressed in association with tau deposits in tauopathies [28].


  1. Linkage disequilibrium and association of MAPT H1 in Parkinson disease. Skipper, L., Wilkes, K., Toft, M., Baker, M., Lincoln, S., Hulihan, M., Ross, O.A., Hutton, M., Aasly, J., Farrer, M. Am. J. Hum. Genet. (2004) [Pubmed]
  2. The structure of the tau haplotype in controls and in progressive supranuclear palsy. Pittman, A.M., Myers, A.J., Duckworth, J., Bryden, L., Hanson, M., Abou-Sleiman, P., Wood, N.W., Hardy, J., Lees, A., de Silva, R. Hum. Mol. Genet. (2004) [Pubmed]
  3. Genomic architecture of human 17q21 linked to frontotemporal dementia uncovers a highly homologous family of low-copy repeats in the tau region. Cruts, M., Rademakers, R., Gijselinck, I., van der Zee, J., Dermaut, B., de Pooter, T., de Rijk, P., Del-Favero, J., van Broeckhoven, C. Hum. Mol. Genet. (2005) [Pubmed]
  4. From fruit fly to bedside: translating lessons from Drosophila models of neurodegenerative disease. Shulman, J.M., Shulman, L.M., Weiner, W.J., Feany, M.B. Curr. Opin. Neurol. (2003) [Pubmed]
  5. Hyperphosphorylation induces self-assembly of tau into tangles of paired helical filaments/straight filaments. Alonso , A., Zaidi, T., Novak, M., Grundke-Iqbal, I., Iqbal, K. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  6. A novel presenilin 1 mutation associated with Pick's disease but not beta-amyloid plaques. Dermaut, B., Kumar-Singh, S., Engelborghs, S., Theuns, J., Rademakers, R., Saerens, J., Pickut, B.A., Peeters, K., van den Broeck, M., Vennekens, K., Claes, S., Cruts, M., Cras, P., Martin, J.J., Van Broeckhoven, C., De Deyn, P.P. Ann. Neurol. (2004) [Pubmed]
  7. Tauopathy in Drosophila: neurodegeneration without neurofibrillary tangles. Wittmann, C.W., Wszolek, M.F., Shulman, J.M., Salvaterra, P.M., Lewis, J., Hutton, M., Feany, M.B. Science (2001) [Pubmed]
  8. More than just two peas in a pod: common amyloidogenic properties of tau and alpha-synuclein in neurodegenerative diseases. Lee, V.M., Giasson, B.I., Trojanowski, J.Q. Trends Neurosci. (2004) [Pubmed]
  9. Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo. Noble, W., Planel, E., Zehr, C., Olm, V., Meyerson, J., Suleman, F., Gaynor, K., Wang, L., LaFrancois, J., Feinstein, B., Burns, M., Krishnamurthy, P., Wen, Y., Bhat, R., Lewis, J., Dickson, D., Duff, K. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  10. O-GlcNAcylation regulates phosphorylation of tau: a mechanism involved in Alzheimer's disease. Liu, F., Iqbal, K., Grundke-Iqbal, I., Hart, G.W., Gong, C.X. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  11. CHIP and Hsp70 regulate tau ubiquitination, degradation and aggregation. Petrucelli, L., Dickson, D., Kehoe, K., Taylor, J., Snyder, H., Grover, A., De Lucia, M., McGowan, E., Lewis, J., Prihar, G., Kim, J., Dillmann, W.H., Browne, S.E., Hall, A., Voellmy, R., Tsuboi, Y., Dawson, T.M., Wolozin, B., Hardy, J., Hutton, M. Hum. Mol. Genet. (2004) [Pubmed]
  12. Comparison of pathways controlling toxicity in the eye and brain in Drosophila models of human neurodegenerative diseases. Ghosh, S., Feany, M.B. Hum. Mol. Genet. (2004) [Pubmed]
  13. Region-specific Dissociation of Neuronal Loss and Neurofibrillary Pathology in a Mouse Model of Tauopathy. Spires, T.L., Orne, J.D., Santacruz, K., Pitstick, R., Carlson, G.A., Ashe, K.H., Hyman, B.T. Am. J. Pathol. (2006) [Pubmed]
  14. Inhibition of heparin-induced tau filament formation by phenothiazines, polyphenols, and porphyrins. Taniguchi, S., Suzuki, N., Masuda, M., Hisanaga, S., Iwatsubo, T., Goedert, M., Hasegawa, M. J. Biol. Chem. (2005) [Pubmed]
  15. Transient cerebral ischemia induces aberrant neuronal cell cycle re-entry and Alzheimer's disease-like tauopathy in female rats. Wen, Y., Yang, S., Liu, R., Brun-Zinkernagel, A.M., Koulen, P., Simpkins, J.W. J. Biol. Chem. (2004) [Pubmed]
  16. Tau pathology in a family with dementia and a P301L mutation in tau. Mirra, S.S., Murrell, J.R., Gearing, M., Spillantini, M.G., Goedert, M., Crowther, R.A., Levey, A.I., Jones, R., Green, J., Shoffner, J.M., Wainer, B.H., Schmidt, M.L., Trojanowski, J.Q., Ghetti, B. J. Neuropathol. Exp. Neurol. (1999) [Pubmed]
  17. Mutations in tau gene exon 10 associated with FTDP-17 alter the activity of an exonic splicing enhancer to interact with Tra2 beta. Jiang, Z., Tang, H., Havlioglu, N., Zhang, X., Stamm, S., Yan, R., Wu, J.Y. J. Biol. Chem. (2003) [Pubmed]
  18. Unique tauopathy in Fukuyama-type congenital muscular dystrophy. Saito, Y., Motoyoshi, Y., Kashima, T., Izumiyama-Shimomura, N., Toda, T., Nakano, I., Hasegawa, M., Murayama, S. J. Neuropathol. Exp. Neurol. (2005) [Pubmed]
  19. Phenotypic heterogeneity of FTDP-17: implications for the differences of pathological phenotype among sporadic tauopathies. Arai, T., Ikeda, K. Neurobiol. Aging (2001) [Pubmed]
  20. General aspects of neurodegeneration. Jellinger, K.A. J. Neural Transm. Suppl. (2003) [Pubmed]
  21. Abnormal Sp1 transcription factor expression in Alzheimer disease and tauopathies. Santpere, G., Nieto, M., Puig, B., Ferrer, I. Neurosci. Lett. (2006) [Pubmed]
  22. Anti-tau phospho-specific Ser262 antibody recognizes a variety of abnormal hyper-phosphorylated tau deposits in tauopathies including Pick bodies and argyrophilic grains. Ferrer, I., Barrachina, M., Puig, B. Acta Neuropathol. (2002) [Pubmed]
  23. Tau aggregation in the hippocampal formation: an ageing or a pathological process? Delacourte, A., Sergeant, N., Wattez, A., Maurage, C.A., Lebert, F., Pasquier, F., David, J.P. Exp. Gerontol. (2002) [Pubmed]
  24. Pathological properties of the Parkinson's disease-associated protein DJ-1 in alpha-synucleinopathies and tauopathies: relevance for multiple system atrophy and Pick's disease. Neumann, M., Müller, V., Görner, K., Kretzschmar, H.A., Haass, C., Kahle, P.J. Acta Neuropathol. (2004) [Pubmed]
  25. Neuronal or glial expression of human apolipoprotein e4 affects parenchymal and vascular amyloid pathology differentially in different brain regions of double- and triple-transgenic mice. Van Dooren, T., Muyllaert, D., Borghgraef, P., Cresens, A., Devijver, H., Van der Auwera, I., Wera, S., Dewachter, I., Van Leuven, F. Am. J. Pathol. (2006) [Pubmed]
  26. Aberrant phosphorylation of alpha-synuclein in human Niemann-Pick type C1 disease. Saito, Y., Suzuki, K., Hulette, C.M., Murayama, S. J. Neuropathol. Exp. Neurol. (2004) [Pubmed]
  27. Ubiquitin-binding protein p62 is present in neuronal and glial inclusions in human tauopathies and synucleinopathies. Kuusisto, E., Salminen, A., Alafuzoff, I. Neuroreport (2001) [Pubmed]
  28. Phosphorylated mitogen-activated protein kinase (MAPK/ERK-P), protein kinase of 38 kDa (p38-P), stress-activated protein kinase (SAPK/JNK-P), and calcium/calmodulin-dependent kinase II (CaM kinase II) are differentially expressed in tau deposits in neurons and glial cells in tauopathies. Ferrer, I., Blanco, R., Carmona, M., Puig, B. Journal of neural transmission (Vienna, Austria : 1996) (2001) [Pubmed]
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