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

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.

Author information

1
Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China. Electronic address: chenxiaowei@nbu.edu.cn.
2
Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.
3
Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China. Electronic address: wangqinwen@nbu.edu.cn.

Abstract

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

[Indexed for MEDLINE]

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