ArticleACS chemical neuroscience2011
A safe, blood-brain barrier permeable triphenylmethane dye inhibits amyloid-β neurotoxicity by generating nontoxic aggregates.
Article in ACS chemical neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Accumulation of amyloid beta in human glioblastomas.Clinical and experimental immunology · 2020Trial
- Retro-Orbital Delivery of AAVs for CNS Wide Astrocyte Targeting.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Leuco Ethyl Violet as Self-Activating Prodrug Photocatalyst for In Vivo Amyloid-Selective Oxygenation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Adenosine triphosphate induces amorphous aggregation of amyloid β by increasing Aβ dynamics.Scientific reports · 2024Article
- A Review of the Association of Blue Food Coloring With Attention Deficit Hyperactivity Disorder Symptoms in Children.Cureus · 2022Review
- RETRACTED: Ameliorative Properties of Boronic Compounds in In Vitro and In Vivo Models of Alzheimer's Disease.International journal of molecular sciences · 2020Article
- Comparing modes of delivery of a combination of ion channel inhibitors for limiting secondary degeneration following partial optic nerve transection.Scientific reports · 2019Article
- A Novel PEGylated Block Copolymer in New Age Therapeutics for Alzheimer's Disease.Molecular neurobiology · 2019Article
- Comparison of ion channel inhibitor combinations for limiting secondary degeneration following partial optic nerve transection.Experimental brain research · 2019Article
- Article
- Repurposing Triphenylmethane Dyes to Bind to Trimers Derived from Aβ.Journal of the American Chemical Society · 2018Article
- Fast Green FCF Alleviates Pain Hypersensitivity and Down-Regulates the Levels of Spinal P2X4 Expression and Pro-inflammatory Cytokines in a Rodent Inflammatory Pain Model.Frontiers in pharmacology · 2018Article
- Article
- Investigation of the effect of erythrosine B on amyloid beta peptide using molecular modeling.Journal of molecular modeling · 2016Article
- The Effects of Latrepirdine on Amyloid-β Aggregation and Toxicity.Journal of Alzheimer's disease : JAD · 2016Article
- Oral Triphenylmethane Food Dye Analog, Brilliant Blue G, Prevents Neuronal Loss in APPSwDI/NOS2-/- Mouse Model.Current Alzheimer research · 2016Article
- P2X7 Receptor Antagonism Attenuates the Intermittent Hypoxia-induced Spatial Deficits in a Murine Model of Sleep Apnea Via Inhibiting Neuroinflammation and Oxidative Stress.Chinese medical journal · 2015Article
- Polyphenols as therapeutic molecules in Alzheimer's disease through modulating amyloid pathways.Molecular neurobiology · 2015Review
- Rationally designed peptoids modulate aggregation of amyloid-beta 40.ACS chemical neuroscience · 2014Article
- Transthyretin-derived peptides as β-amyloid inhibitors.ACS chemical neuroscience · 2014Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing evidence suggests that on-pathway amyloid-β (Aβ) oligomers are primary neurotoxic species and have a direct correlation with the onset of Alzheimer's disease (AD). One promising therapeutic strategy to block AD progression is to reduce the levels of these neurotoxic Aβ species using small molecules. While several compounds have been shown to modulate Aβ aggregation, compounds with such activity combined with safety and high blood-brain barrier (BBB) permeability have yet to be reported. Brilliant Blue G (BBG) is a close structural analogue of a U.S. Food and Drug Administration (FDA)-approved food dye and has recently garnered prominent attention as a potential drug to treat spinal cord injury due to its neuroprotective effects along with BBB permeability and high degree of safety. In this work, we demonstrate that BBG is an effective Aβ aggregation modulator, which reduces Aβ-associated cytotoxicity in a dose-dependent manner by promoting the formation of off-pathway, nontoxic aggregates. Comparative studies of BBG and three structural analogues, Brilliant Blue R (BBR), Brilliant Blue FCF (BBF), and Fast Green FCF (FGF), revealed that BBG is most effective, BBR is moderately effective, and BBF and FGF are least effective in modulating Aβ aggregation and cytotoxicity. Therefore, the two additional methyl groups of BBG and other structural differences between the congeners are important in the interaction of BBG with Aβ leading to formation of nontoxic Aβ aggregates. Our findings support the hypothesis that generating nontoxic aggregates using small molecule modulators is an effective strategy for reducing Aβ cytotoxicity. Furthermore, key structural features of BBG identified through structure-function studies can open new avenues into therapeutic design for combating AD.
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