In recent years, Brilliant Blue G (BBG), a triphenylmethane dye which is a close structural analog of a Food and Drug Administration (FDA)-approved food dye, has drawn prominent attention as a potential drug to treat neurodegenerative disorders. Accumulating evidence demonstrates that the neuroprotective effect of BBG strongly associates with antagonizing the purinergic P2X7 receptor, a non-selective ligand-gated ion channel activated by extracellular ATP. Activation of P2X7 receptor is responsible for glial activation and release of the pro-inflammatory cytokines as interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF-α), that lead to neuroinflammatory reaction and greatly contribute to progressing of neurodegenerative diseases. Pharmacologically inactivating P2X7 receptors by BBG has proven anti-inflammatory effects both in vivo and in vitro . Growing evidence presents that BBG reduces neuronal death, inhibits release of inflammatory factors not only in AD but also in ischemia, Huntington’s disease (HD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS).
In this study the authors report that systematic administration of BBG diminishes spatial memory impairment and cognitive deficits in a mouse AD model produced by injecting soluble Aβ peptide into the hippocampal CA1 region. In addition, the data show that Aβ-induced loss of filopodia and spine density in cultured hippocampal neurons was prevented by administration of BBG. Based on these, and other data, the authors conclude that BBG prevents the learning and memory impairment and cognitive deficits induced by the toxicity of soluble Aβ, 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, the data suggest a potential for BBG as a new therapy for AD.