| First Author | Chen X | Year | 2014 |
| Journal | Neuroscience | Volume | 279 |
| Pages | 94-101 | PubMed ID | 25193238 |
| Mgi Jnum | J:215899 | Mgi Id | MGI:5607334 |
| Doi | 10.1016/j.neuroscience.2014.08.036 | Citation | Chen X, et al. (2014) Brilliant Blue G improves cognition in an animal model of Alzheimer's disease and inhibits amyloid-beta-induced loss of filopodia and dendrite spines in hippocampal neurons. Neuroscience 279:94-101 |
| abstractText | Deposits of amyloid-beta (Abeta) protein are one of the hallmarks of Alzheimer''s disease (AD). Numerous studies report that the Abeta peptide, especially in the oligomeric form, causes memory decline and other cognitive deficits. However, there have been very few effective interventions for termination or even delay of AD progression. Brilliant Blue G (BBG), a safe triphenylmethane dye and P2X7 antagonist, has been reported to have protective effects on neuroinflammation, ischemia, spinal injury and neurodegenerative disorders. Here we report that systematic administration of BBG diminishes spatial memory impairment and cognitive deficits in a mouse AD model produced by injecting soluble Abeta peptide into the hippocampal CA1 region. In addition, we show that Abeta-induced loss of filopodia and spine density in cultured hippocampal neurons was prevented by administration of BBG. We conclude that BBG prevents the learning and memory impairment and cognitive deficits induced by the toxicity of soluble Abeta, and improves the development of dendritic spines in hippocampal neurons in an AD model mouse. Considering the safety and blood-brain-barrier (BBB)-permeability of BBG, our data suggest a potential for BBG as a new therapy for AD. |
