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Oligomeric Amyloid-β Toxicity Can Be Inhibited by Blocking Its Cellular Binding in Cortical Neuronal Cultures with Addition of the Triphenylmethane Dye Brilliant Blue G.
ACS Chem Neurosci 2016; 7(8):1141-7AC

Abstract

Accumulation of soluble amyloid β (Aβ) oligomers in the brain has been suggested to cause neurodegeneration associated with Alzheimer's disease (AD). Our previous findings showed that the binding of Aβ trimer and tetramer to neurons is significantly correlated with Aβ-induced neuronal cell death. We propose blocking of neuronal binding of these neurotoxic Aβ oligomers as a therapeutic strategy for preventing this disease. To test this, a nontoxic triphenylmethane dye, Brilliant Blue G (BBG), which has been reported to modulate Aβ aggregation and neurotoxicity, was investigated using mouse primary cortical neuronal cultures treated with photoinduced cross-linked toxic Aβ40 oligomers as well as soluble Aβ40 and Aβ42 peptides. We found that the BBG-induced decrease in Aβ binding resulted in a significant decrease in its neurotoxicity. These findings support our hypothesis that disruption of cellular Aβ binding is a promising therapeutic strategy for combating AD.

Authors+Show Affiliations

Department of Pathology, The University of Melbourne , Parkville, VIC 3010, Australia.Department of Pathology, The University of Melbourne , Parkville, VIC 3010, Australia.Department of Pathology, The University of Melbourne , Parkville, VIC 3010, Australia.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27258855

Citation

Jana, Metta K., et al. "Oligomeric Amyloid-β Toxicity Can Be Inhibited By Blocking Its Cellular Binding in Cortical Neuronal Cultures With Addition of the Triphenylmethane Dye Brilliant Blue G." ACS Chemical Neuroscience, vol. 7, no. 8, 2016, pp. 1141-7.
Jana MK, Cappai R, Ciccotosto GD. Oligomeric Amyloid-β Toxicity Can Be Inhibited by Blocking Its Cellular Binding in Cortical Neuronal Cultures with Addition of the Triphenylmethane Dye Brilliant Blue G. ACS Chem Neurosci. 2016;7(8):1141-7.
Jana, M. K., Cappai, R., & Ciccotosto, G. D. (2016). Oligomeric Amyloid-β Toxicity Can Be Inhibited by Blocking Its Cellular Binding in Cortical Neuronal Cultures with Addition of the Triphenylmethane Dye Brilliant Blue G. ACS Chemical Neuroscience, 7(8), pp. 1141-7. doi:10.1021/acschemneuro.6b00108.
Jana MK, Cappai R, Ciccotosto GD. Oligomeric Amyloid-β Toxicity Can Be Inhibited By Blocking Its Cellular Binding in Cortical Neuronal Cultures With Addition of the Triphenylmethane Dye Brilliant Blue G. ACS Chem Neurosci. 2016 08 17;7(8):1141-7. PubMed PMID: 27258855.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oligomeric Amyloid-β Toxicity Can Be Inhibited by Blocking Its Cellular Binding in Cortical Neuronal Cultures with Addition of the Triphenylmethane Dye Brilliant Blue G. AU - Jana,Metta K, AU - Cappai,Roberto, AU - Ciccotosto,Giuseppe D, Y1 - 2016/06/10/ PY - 2016/6/4/entrez PY - 2016/6/4/pubmed PY - 2017/10/31/medline KW - Alzheimer’s disease (AD) KW - PICUP KW - amyloid β (Aβ) KW - brilliant blue G KW - oligomer KW - tetramer KW - toxicity SP - 1141 EP - 7 JF - ACS chemical neuroscience JO - ACS Chem Neurosci VL - 7 IS - 8 N2 - Accumulation of soluble amyloid β (Aβ) oligomers in the brain has been suggested to cause neurodegeneration associated with Alzheimer's disease (AD). Our previous findings showed that the binding of Aβ trimer and tetramer to neurons is significantly correlated with Aβ-induced neuronal cell death. We propose blocking of neuronal binding of these neurotoxic Aβ oligomers as a therapeutic strategy for preventing this disease. To test this, a nontoxic triphenylmethane dye, Brilliant Blue G (BBG), which has been reported to modulate Aβ aggregation and neurotoxicity, was investigated using mouse primary cortical neuronal cultures treated with photoinduced cross-linked toxic Aβ40 oligomers as well as soluble Aβ40 and Aβ42 peptides. We found that the BBG-induced decrease in Aβ binding resulted in a significant decrease in its neurotoxicity. These findings support our hypothesis that disruption of cellular Aβ binding is a promising therapeutic strategy for combating AD. SN - 1948-7193 UR - https://www.unboundmedicine.com/medline/citation/27258855/Oligomeric_Amyloid_β_Toxicity_Can_Be_Inhibited_by_Blocking_Its_Cellular_Binding_in_Cortical_Neuronal_Cultures_with_Addition_of_the_Triphenylmethane_Dye_Brilliant_Blue_G_ L2 - https://dx.doi.org/10.1021/acschemneuro.6b00108 DB - PRIME DP - Unbound Medicine ER -