Neuroprotective action of proline-rich polypeptide-1 in β-amyloid induced neurodegeneration in rats

被引:28
|
作者
Yenkoyan, Konstantin [1 ]
Safaryan, Karen [2 ]
Chavushyan, Vergine [3 ]
Meliksetyan, Irina [4 ]
Navasardyan, Grizelda [5 ]
Sarkissian, John [3 ]
Galoyan, Armen [6 ]
Aghajanov, Michail [1 ]
机构
[1] Yerevan State Med Univ M Heratsi, Dept Biochem, Yerevan 0025, Armenia
[2] Univ Hertfordshire, Biol & Neural Computat Grp, Hatfield AL10 9AB, Herts, England
[3] NAS RA, L Orbeli Inst Physiol, Lab Physiol Compensat CNS Funct, Yerevan, Armenia
[4] NAS RA, L Orbeli Inst Physiol, Neuromorphol Lab, Yerevan, Armenia
[5] Yerevan State Med Univ M Heratsi, Dept Pathophysiol, Yerevan 0025, Armenia
[6] NAS RA, H Buniatyan Inst Biochem, Lab Neurohormones, Yerevan, Armenia
关键词
Neurodegeneration; beta-Amyloid; PRP-1; Neuroprotection; ALZHEIMERS-DISEASE; HYPOTHALAMIC PEPTIDE; SYNAPTIC PLASTICITY; MOLECULAR-BASIS; MEMORY; BRAIN; OLIGOMERS; INHIBITION; PATHOLOGY; SYNAPSES;
D O I
10.1016/j.brainresbull.2011.08.003
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
It is recognized that the main trigger of Alzheimer disease related neurodegeneration is beta-amyloid peptide, which subsequently generates different metabolic disorders in neuron and finally leads to neuronal death. Several biologically active products were tested as neuroprotectors, but only few of them demonstrated any efficiency. Proline-rich polypeptide-1 was tested as a neuroprotective agent on A beta 25-35 animal model of Alzheimer disease. Biochemical analysis (determination of spectrum of neuroactive amino acids, such as glutamate, gamma-aminobutyric acid, glycine, aspartate and taurine), as well as behavioral, electrophysiological and morphological studies were performed to reveal the neuroprotective potential of proline-rich polypeptide in rats. Based on the results of our study it can be concluded that praline-rich polypeptide-1 has a potential to be one of the effective preventive or therapeutic agents against neurodegenerative disorders, such as Alzheimer disease. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:262 / 271
页数:10
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