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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


Year of Publication:
Contact PI Name:
Xiaowei Chen
Contact PI Affiliation:
School of Medicine, Ningbo University, Ningbo, China
J. Hu, L. Jiang, S. Xu, B. Zheng, C. Wang, J. Zhang, X. Wei, L. Chang, Q. Wang
Primary Reference (PubMED ID):
Funding Source:
Ministry of Science and Technology of China
National Natural Science Foundation of China
Ningbo Key Science and Technology Project
Ningbo Natural Science Foundation
Study Goal and Principal Findings:

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.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Small Molecule
Therapeutic Agent:
Brilliant Blue G (BBG)
Therapeutic Target:
P2X7 Purinergic Receptor

Animal Model

Model Information:
Model Type:
beta Amyloid Peptide Injection
Strain/Genetic Background:
Model Type:
Strain/Genetic Background:
Not Applicable

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest


Outcome Measured
Outcome Parameters
Morris Water Maze
Novel Object Recognition Test (NORT)
Dendritic Spines
Dendritic Filopodia Density