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Chemical Compound Review

THIOFLAVIN     2-phenylthiochroman

Synonyms: SureCN44650, AG-G-12586, CTK5B0209, AC1L2K18, 5961-99-9, ...
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Disease relevance of THIOFLAVIN

  • We found dramatic, focal neuronal toxicity associated primarily with thioflavin S-positive fibrillar Abeta deposits in both AD and PSAPP mice [1].
  • The geometry of the hearts and ischemic zones was preserved, the margins of ischemia being defined as the outer border of Thioflavin S nonfluorescence [2].
  • In the current study, we used BSB to probe postmortem tissues from patients with various neurodegenerative diseases with diagnostic lesions characterized by fibrillar intra- or extracellular lesions and compared these results with standard histochemical dyes such as thioflavin S and immunohistochemical stains specific for the same lesions [3].
  • In five groups of anesthetized, open-chest rabbits (30-min coronary occlusion and different durations of reperfusion), anatomic no reflow was determined by injection of thioflavin S at the end of reperfusion and compared with regional myocardial blood flow (RMBF; radioactive microspheres) and infarct size (triphenyltetrazolium) [4].
  • Transgenic mice overexpressing TGF-beta1 in astrocytes develop AD-like cerebrovascular abnormalities, including perivascular astrocytosis, microvascular basement membrane thickening, and accumulation of thioflavin S-positive amyloid in the absence of parenchymal degeneration [5].

Psychiatry related information on THIOFLAVIN

  • In a study of 32 brains obtained from patients with Alzheimer's disease (AD), thioflavin S-stained sections from the PAG contained major pathological changes in 81% of cases [6].

High impact information on THIOFLAVIN

  • A subset of these deposits also bind the amyloid-specific dye thioflavin S, indicating that these deposits have the tinctural characteristics of classic amyloid [7].
  • The synthetic PHFs bound the dye thioflavin S used in Alzheimer disease diagnostics [8].
  • Severe depression of regional blood flow during reperfusion was present within the infarcted tissue and was associated with an anatomic perfusion defect as defined by thioflavin S; there was moderate depression of flow within the noninfarcted, salvaged subepicardium [9].
  • Propranolol also limited microvascular injury so that perfusion defects, detected with the dye thioflavin S, were smaller in treated dogs [10].
  • Of the 20 samples from Nairobi, 3 (15%) brains exhibited neocortical A beta deposits that varied from numerous diffuse to highly localized compact or neuritic plaques, many of which were also thioflavin S positive [11].

Chemical compound and disease context of THIOFLAVIN


Biological context of THIOFLAVIN

  • Thioflavin S histochemistry suggested accumulations of amyloid in the cerebrovasculature of transgenic mice with the highest expression of the beta APP-C100 transgene [13].
  • Actinomycin D, but not a caspase inhibitor, prevented inclusion formation, whereas both agents inhibited cell death. alpha-Synuclein and thioflavin S staining were found within the inclusions. alpha-Synuclein, however, did not appear to be ubiquitinated or aggregated [14].
  • Studies of the interaction of these complexes and of the dyes with the pBR322 plasmid superhelical DNA demonstrated that while each complex and dye readily associated with the DNA in a dose-dependent manner, only Pt(Thioflavin)2 and Thioflavin produced irreversible DNA changes (single-strand breaks) [15].

Anatomical context of THIOFLAVIN


Associations of THIOFLAVIN with other chemical compounds


Gene context of THIOFLAVIN

  • The measures of Abeta deposition, Abeta-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Abeta, failed to distinguish HPC from AD patients and were poor correlates of synaptic change [26].
  • Also, SAP and C1q enhanced PrP-peptide fibril formation as revealed by electron microscopy and thioflavin S-based quantitative assays [27].
  • Neuritic plaques identified on double label experiments with thioflavin include somatostatin axons but not neurons [28].
  • Amyloid burden, expressed as the percentage area occupied by thioflavin S-positive amyloid deposits, increased an average of 179-fold from 12 to 54 weeks of age (0.02+/-0.01% to 3.57+/-0.29%, mean+/-S.E.M., respectively) in five regions of the cortex and two of the hippocampus [29].
  • Electron microscopy and thioflavin S reactivity of the fractions show that the juxtanuclear inclusion bodies are filled with amyloid-like alpha-synuclein fibrils, whereas both the small aggregate fractions contain non-fibrillar spherical aggregates with distinct size distributions [30].

Analytical, diagnostic and therapeutic context of THIOFLAVIN

  • The area of impaired perfusion (absent thioflavin) averaged 9.5 +/- 3.0% of the risk region in dogs reperfused for 2 minutes, whereas it was nearly three times as large in dogs reperfused for 3.5 hours (25.9 +/- 8.2% of the risk region, p less than 0.05) [31].
  • The MRI hypoenhanced region increased 3-fold during 48 hours after reperfusion (3.2+/-1.8%, 6.7+/-4.4%, and 9.9+/-3.2% of left ventricular mass at 2, 6, and 48 hours, respectively, P<0.03) and correlated well with microvascular obstruction (MBF <50% of remote region, r=0.99 and thioflavin S, r=0.93) [32].
  • The filamentous nature of these thioflavin-binding amyloid polymers was verified by electron microscopy [33].
  • The histopathology of senile plaques was studied using double-labeling immunohistochemistry and lectin histochemistry with thioflavin S fluorescent microscopy in 9 cases of Alzheimer's disease, 2 nondemented elderly individuals, and 3 individuals with non-Alzheimer primary degenerative dementias [17].
  • The severity of ischemia was determined by the radioactive microsphere and thioflavin S techniques [34].


  1. Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease. Urbanc, B., Cruz, L., Le, R., Sanders, J., Ashe, K.H., Duff, K., Stanley, H.E., Irizarry, M.C., Hyman, B.T. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  2. A solid angle analysis of the epicardial ischemic TQ-ST deflection in the pig. A theoretical and experimental study. Richeson, J.F., Akiyama, T., Schenk, E. Circ. Res. (1978) [Pubmed]
  3. The fluorescent Congo red derivative, (trans, trans)-1-bromo-2,5-bis-(3-hydroxycarbonyl-4-hydroxy)styrylbenzene (BSB), labels diverse beta-pleated sheet structures in postmortem human neurodegenerative disease brains. Schmidt, M.L., Schuck, T., Sheridan, S., Kung, M.P., Kung, H., Zhuang, Z.P., Bergeron, C., Lamarche, J.S., Skovronsky, D., Giasson, B.I., Lee, V.M., Trojanowski, J.Q. Am. J. Pathol. (2001) [Pubmed]
  4. Microvascular reperfusion injury: rapid expansion of anatomic no reflow during reperfusion in the rabbit. Reffelmann, T., Kloner, R.A. Am. J. Physiol. Heart Circ. Physiol. (2002) [Pubmed]
  5. Molecular and functional dissection of TGF-beta1-induced cerebrovascular abnormalities in transgenic mice. Buckwalter, M., Pepper, J.P., Gaertner, R.F., Von Euw, D., Lacombe, P., Wyss-Coray, T. Ann. N. Y. Acad. Sci. (2002) [Pubmed]
  6. Selective pathological changes of the periaqueductal gray matter in Alzheimer's disease. Parvizi, J., Van Hoesen, G.W., Damasio, A. Ann. Neurol. (2000) [Pubmed]
  7. Expression of human beta-amyloid peptide in transgenic Caenorhabditis elegans. Link, C.D. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  8. Oxidation of cysteine-322 in the repeat domain of microtubule-associated protein tau controls the in vitro assembly of paired helical filaments. Schweers, O., Mandelkow, E.M., Biernat, J., Mandelkow, E. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  9. The effect of streptokinase on intramyocardial hemorrhage, infarct size, and the no-reflow phenomenon during coronary reperfusion. Kloner, R.A., Alker, K.J. Circulation (1984) [Pubmed]
  10. Infarct size reduction by propranolol before and after coronary ligation in dogs. Rasmussen, M.M., Reimer, K.A., Kloner, R.A., Jennings, R.B. Circulation (1977) [Pubmed]
  11. Cerebral amyloid beta protein deposits and other Alzheimer lesions in non-demented elderly east Africans. Ogeng'o, J.A., Cohen, D.L., Sayi, J.G., Matuja, W.B., Chande, H.M., Kitinya, J.N., Kimani, J.K., Friedland, R.P., Mori, H., Kalaria, R.N. Brain Pathol. (1996) [Pubmed]
  12. Congo red staining on 1 micron de-plasticized sections for detection of lesions in Alzheimer's disease and related disorders. Snow, A.D., Mar, H., Nochlin, D., Wight, T.N. Prog. Clin. Biol. Res. (1989) [Pubmed]
  13. Deposition of beta/A4 immunoreactivity and neuronal pathology in transgenic mice expressing the carboxyl-terminal fragment of the Alzheimer amyloid precursor in the brain. Kammesheidt, A., Boyce, F.M., Spanoyannis, A.F., Cummings, B.J., Ortegón, M., Cotman, C., Vaught, J.L., Neve, R.L. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  14. Proteasomal inhibition-induced inclusion formation and death in cortical neurons require transcription and ubiquitination. Rideout, H.J., Stefanis, L. Mol. Cell. Neurosci. (2002) [Pubmed]
  15. Cytotoxicity, radiosensitization, and DNA interaction of platinum complexes of thiazin and xanthene dyes. Teicher, B.A., Herman, T.S., Kaufmann, M.E. Radiat. Res. (1990) [Pubmed]
  16. Precordial and epicardial surface potentials during Myocardial ischemia in the pig. A theoretical and experimental analysis of the TQ and ST segments. Holland, R.P., Brooks, H. Circ. Res. (1975) [Pubmed]
  17. Alzheimer's disease. A double-labeling immunohistochemical study of senile plaques. Dickson, D.W., Farlo, J., Davies, P., Crystal, H., Fuld, P., Yen, S.H. Am. J. Pathol. (1988) [Pubmed]
  18. Tau assembly in inducible transfectants expressing wild-type or FTDP-17 tau. DeTure, M., Ko, L.W., Easson, C., Yen, S.H. Am. J. Pathol. (2002) [Pubmed]
  19. Formation and removal of alpha-synuclein aggregates in cells exposed to mitochondrial inhibitors. Lee, H.J., Shin, S.Y., Choi, C., Lee, Y.H., Lee, S.J. J. Biol. Chem. (2002) [Pubmed]
  20. Mostly separate distributions of CLAC- versus Abeta40- or thioflavin S-reactivities in senile plaques reveal two distinct subpopulations of beta-amyloid deposits. Kowa, H., Sakakura, T., Matsuura, Y., Wakabayashi, T., Mann, D.M., Duff, K., Tsuji, S., Hashimoto, T., Iwatsubo, T. Am. J. Pathol. (2004) [Pubmed]
  21. Immunohistochemical colocalization of amyloid precursor protein with cerebrovascular amyloid of Alzheimer's disease. Ko, L.W., Sheu, K.F., Blass, J.P. Am. J. Pathol. (1991) [Pubmed]
  22. Anthraquinones inhibit tau aggregation and dissolve Alzheimer's paired helical filaments in vitro and in cells. Pickhardt, M., Gazova, Z., von Bergen, M., Khlistunova, I., Wang, Y., Hascher, A., Mandelkow, E.M., Biernat, J., Mandelkow, E. J. Biol. Chem. (2005) [Pubmed]
  23. Parkin accumulation in aggresomes due to proteasome impairment. Junn, E., Lee, S.S., Suhr, U.T., Mouradian, M.M. J. Biol. Chem. (2002) [Pubmed]
  24. Progressive failure of coronary flow during reperfusion of myocardial infarction: documentation of the no reflow phenomenon with positron emission tomography. Jeremy, R.W., Links, J.M., Becker, L.C. J. Am. Coll. Cardiol. (1990) [Pubmed]
  25. Triggers of full-length tau aggregation: a role for partially folded intermediates. Chirita, C.N., Congdon, E.E., Yin, H., Kuret, J. Biochemistry (2005) [Pubmed]
  26. Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease. Lue, L.F., Kuo, Y.M., Roher, A.E., Brachova, L., Shen, Y., Sue, L., Beach, T., Kurth, J.H., Rydel, R.E., Rogers, J. Am. J. Pathol. (1999) [Pubmed]
  27. Activation of human microglia by fibrillar prion protein-related peptides is enhanced by amyloid-associated factors SAP and C1q. Veerhuis, R., Boshuizen, R.S., Morbin, M., Mazzoleni, G., Hoozemans, J.J., Langedijk, J.P., Tagliavini, F., Langeveld, J.P., Eikelenboom, P. Neurobiol. Dis. (2005) [Pubmed]
  28. Somatostatin immunoreactive neurons in the human hippocampus and cortex shown by immunogold/silver intensification on vibratome sections: coexistence with neuropeptide Y neurons, and effects in Alzheimer-type dementia. Chan-Palay, V. J. Comp. Neurol. (1987) [Pubmed]
  29. Quantitative histological analysis of amyloid deposition in Alzheimer's double transgenic mouse brain. Wengenack, T.M., Whelan, S., Curran, G.L., Duff, K.E., Poduslo, J.F. Neuroscience (2000) [Pubmed]
  30. Characterization of cytoplasmic alpha-synuclein aggregates. Fibril formation is tightly linked to the inclusion-forming process in cells. Lee, H.J., Lee, S.J. J. Biol. Chem. (2002) [Pubmed]
  31. Progressive impairment of regional myocardial perfusion after initial restoration of postischemic blood flow. Ambrosio, G., Weisman, H.F., Mannisi, J.A., Becker, L.C. Circulation (1989) [Pubmed]
  32. Magnitude and time course of microvascular obstruction and tissue injury after acute myocardial infarction. Rochitte, C.E., Lima, J.A., Bluemke, D.A., Reeder, S.B., McVeigh, E.R., Furuta, T., Becker, L.C., Melin, J.A. Circulation (1998) [Pubmed]
  33. Free fatty acids stimulate the polymerization of tau and amyloid beta peptides. In vitro evidence for a common effector of pathogenesis in Alzheimer's disease. Wilson, D.M., Binder, L.I. Am. J. Pathol. (1997) [Pubmed]
  34. Redistribution of catecholamines in the ischemic zone of the dog heart. Muntz, K.H., Hagler, H.K., Boulas, H.J., Willerson, J.T., Buja, L.M. Am. J. Pathol. (1984) [Pubmed]
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