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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.
Neuroscience 2014; 279:94-101N

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.

Authors+Show Affiliations

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.Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory or Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.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.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25193238

Citation

Chen, X, et al. "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, vol. 279, 2014, pp. 94-101.
Chen X, Hu J, Jiang L, et al. 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;279:94-101.
Chen, X., Hu, J., Jiang, L., Xu, S., Zheng, B., Wang, C., ... Wang, Q. (2014). 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, 279, pp. 94-101. doi:10.1016/j.neuroscience.2014.08.036.
Chen X, et al. 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. PubMed PMID: 25193238.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Chen,X, AU - Hu,J, AU - Jiang,L, AU - Xu,S, AU - Zheng,B, AU - Wang,C, AU - Zhang,J, AU - Wei,X, AU - Chang,L, AU - Wang,Q, Y1 - 2014/09/03/ PY - 2014/05/08/received PY - 2014/08/18/revised PY - 2014/08/23/accepted PY - 2014/9/7/entrez PY - 2014/9/7/pubmed PY - 2015/7/15/medline KW - Alzheimer’s disease KW - amyloid KW - hippocampus KW - memory KW - purinergic SP - 94 EP - 101 JF - Neuroscience JO - Neuroscience VL - 279 N2 - 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. SN - 1873-7544 UR - https://www.unboundmedicine.com/medline/citation/25193238/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_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(14)00713-1 DB - PRIME DP - Unbound Medicine ER -