Brilliant Blue G improves cognition in an animal model of Alzheimer's disease and inhibits amyloid-β-induced loss of filopodia and dendrite spines in hippocampal neurons

Neuroscience. 2014 Oct 24;279:94-101. doi: 10.1016/j.neuroscience.2014.08.036. Epub 2014 Sep 3.


Deposits of amyloid-β (Aβ) protein are one of the hallmarks of Alzheimer's disease (AD). Numerous studies report that the Aβ 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 Aβ peptide into the hippocampal CA1 region. In addition, we show that Aβ-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 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, our data suggest a potential for BBG as a new therapy for AD.

Keywords: Alzheimer’s disease; amyloid; hippocampus; memory; purinergic.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / physiopathology
  • Amyloid beta-Peptides
  • Animals
  • Animals, Newborn
  • Cells, Cultured
  • Cognition / drug effects*
  • Cognition / physiology
  • Cognition Disorders / physiopathology
  • Cognition Disorders / prevention & control
  • Dendritic Spines / drug effects
  • Dendritic Spines / physiology
  • Disease Models, Animal
  • Hippocampus / drug effects*
  • Hippocampus / physiopathology
  • Mice, Inbred ICR
  • Neuroprotective Agents / pharmacology*
  • Nootropic Agents / pharmacology*
  • Peptide Fragments
  • Pseudopodia / drug effects
  • Pseudopodia / physiology
  • Rats, Sprague-Dawley
  • Rosaniline Dyes / pharmacology*
  • Spatial Memory / drug effects
  • Spatial Memory / physiology


  • Amyloid beta-Peptides
  • Neuroprotective Agents
  • Nootropic Agents
  • Peptide Fragments
  • Rosaniline Dyes
  • amyloid beta-protein (1-42)
  • coomassie Brilliant Blue