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Chemical Compound Review

CHEMBL57267     4-(3,6-dimethylbenzothiazol- 2-yl)-N,N...

Synonyms: SureCN1577265, CHEBI:76034, CHEBI:188022, STOCK1S-54958, STL058959, ...
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Disease relevance of Setoflavin T


Psychiatry related information on Setoflavin T


High impact information on Setoflavin T

  • The mutants 15Ure2 and Delta 15-42Ure2 showed the same time-dependent variation in fibril types but with an increased lag time detected by ThT binding compared with wild-type Ure2 [3].
  • The results imply a role of the conserved region in both amyloid nucleation and formation of the binding surface recognized by ThT [3].
  • In addition, Delta 15-42Ure2 showed reduced binding to ThT [3].
  • Interleukin-1beta- and tumor necrosis factor alpha-immunopositive microglia were localized with thioflavine-positive (fibrillar) Abeta deposits [4].
  • We counted plaque number, NFT number, dystrophic neurite number, and the relative extent of thioflavine positive plaques and neuritic involvement within plaques [5].

Anatomical context of Setoflavin T


Associations of Setoflavin T with other chemical compounds


Gene context of Setoflavin T

  • Silver and thioflavine staining confirmed the reduction of amyloid plaques on the side of deafferentation [11].
  • CONCLUSIONS: The present data demonstrating amyloidophilic dye binding, in situ red shift in thioflavine fluorescence, and apple-green birefringence provide evidence that lens protein beta-sheet arrays are organized in an amyloid-like supramolecular order in interior fiber cells of mammalian ocular lenses [12].
  • Two techniques were used simultaneously on serial sections: thioflavine staining of amyloid substance and immunohistochemistry with immune sera against Paired Helical Filaments (anti-PHF) and native Tau proteins (anti-Tau) [13].

Analytical, diagnostic and therapeutic context of Setoflavin T

  • Atomic force microscopy height images at successive time points during a single growth experiment showed the sequential appearance of at least four fibril types that could be readily differentiated by height (5, 8, 12, or 9 nm), morphology (twisted or smooth), and/or time of appearance (early or late in the plateau phase of ThT binding) [3].
  • Fibrillization of the neuron-derived diffuse, thioflavine-negative or benign plaques is poor or undetectable by current morphological methods including ultrastructural immunocytochemistry [14].


  1. Tumor-like amyloid formation (amyloidoma) in the brain. Spaar, F.W., Goebel, H.H., Volles, E., Wickboldt, J. J. Neurol. (1981) [Pubmed]
  2. Progressive transformation of the cytoskeleton associated with normal aging and Alzheimer's disease. Vickers, J.C., Delacourte, A., Morrison, J.H. Brain Res. (1992) [Pubmed]
  3. Amyloid nucleation and hierarchical assembly of Ure2p fibrils. Role of asparagine/glutamine repeat and nonrepeat regions of the prion domains. Jiang, Y., Li, H., Zhu, L., Zhou, J.M., Perrett, S. J. Biol. Chem. (2004) [Pubmed]
  4. Evidence for glial-mediated inflammation in aged APP(SW) transgenic mice. Benzing, W.C., Wujek, J.R., Ward, E.K., Shaffer, D., Ashe, K.H., Younkin, S.G., Brunden, K.R. Neurobiol. Aging (1999) [Pubmed]
  5. Beta-amyloid deposition and other measures of neuropathology predict cognitive status in Alzheimer's disease. Cummings, B.J., Pike, C.J., Shankle, R., Cotman, C.W. Neurobiol. Aging (1996) [Pubmed]
  6. Increased immunoreactivity for Jun- and Fos-related proteins in Alzheimer's disease: association with pathology. Anderson, A.J., Cummings, B.J., Cotman, C.W. Exp. Neurol. (1994) [Pubmed]
  7. The presence of isoaspartic acid in beta-amyloid plaques indicates plaque age. Fonseca, M.I., Head, E., Velazquez, P., Cotman, C.W., Tenner, A.J. Exp. Neurol. (1999) [Pubmed]
  8. Transformation of degenerating neurofibrils into amyloid substance in Alzheimer's disease: histochemical and immunohistochemical studies. Défossez, A., Delacourte, A. J. Neurol. Sci. (1987) [Pubmed]
  9. Beta-protein immunoreactivity in the human brain after cardiac arrest. Wiśniewski, H.M., Maślińska, D. Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences. (1996) [Pubmed]
  10. Amyloid neuropathy: a retrospective study of 35 peripheral nerve biopsies. Vital, C., Vital, A., Bouillot-Eimer, S., Brechenmacher, C., Ferrer, X., Lagueny, A. J. Peripher. Nerv. Syst. (2004) [Pubmed]
  11. Disruption of corticocortical connections ameliorates amyloid burden in terminal fields in a transgenic model of Abeta amyloidosis. Sheng, J.G., Price, D.L., Koliatsos, V.E. J. Neurosci. (2002) [Pubmed]
  12. Amyloid-like protein structure in mammalian ocular lenses. Frederikse, P.H. Curr. Eye Res. (2000) [Pubmed]
  13. Cortical angiopathy in Alzheimer's disease: the formation of dystrophic perivascular neurites is related to the exudation of amyloid fibrils from the pathological vessels. Peers, M.C., Lenders, M.B., Défossez, A., Delacourte, A., Mazzuca, M. Virchows Archiv. A, Pathological anatomy and histopathology. (1988) [Pubmed]
  14. Review. David Oppenheimer Memorial Lecture 1995: Some neuropathological aspects of Alzheimer's disease and its relevance to other disciplines. Wisniewski, H.M., Wegiel, J., Kotula, L. Neuropathol. Appl. Neurobiol. (1996) [Pubmed]
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