NEURODEGENERATIVE CHANGES INDUCED BY INJECTION OF beta-AMYLOID PEPTIDE FRAGMENT (25-35) IN HIPPOCAMPUS ARE ASSOCIATED WITH NGF-SIGNALLING ACTIVATION

被引：0
|
作者：
Stepanichev, M. Yu [1 ]
Ivanov, A. D. [1 ]
Lazareva, N. A. [1 ]
Moiseeva, Yu, V [1 ]
Gulyaeva, N., V [1 ]
机构：
[1] Russian Acad Sci, Inst Higher Nervous Act & Neurophysiol, Funct Biochem Nervous Syst Lab, Moscow, Russia
来源：
BULLETIN OF RUSSIAN STATE MEDICAL UNIVERSITY | 2016年 / 01期
基金：
俄罗斯基础研究基金会;
关键词：
beta-amyloid peptide; hippocampus; nerve growth factor; p75NTR receptor; neurodegeneration; Alzheimer's disease;
D O I：
10.24075/brsmu.2016-01-02
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
beta-amyloid peptide (Alpha beta) is an important component of the neurodegeneration mechanism in Alzheimer's disease. This work investigates the effect of intrahippocampal injection of Alpha beta(25-35) fragment on nerve growth factor (NGF) signalling. Aggregated Alpha beta(25-35) was injected into rat dorsal hippocampus. Rats in the control group received injections of the peptide with an inverted amino acid sequence and a solvent. It was shown that Alpha beta(25-35) induces neuron death in rat hippocampus. Neurodegeneration was accompanied by a statistically significant increase (p < 0.05) in p75NTR neurotrophin receptor expression in all animals who had received exogenous peptides, and by an increased level of NGF in the hippocampus of those rats who had been injected with Alpha beta(25-35). The study results demonstrate that changes in the hippocampus induced by Alpha beta(25-35) are accompanied by increased NGF signalling, which, to some extent, supports the current clinical data obtained from patients with Alzheimer's. The changes mentioned above are compensatory. However, both damage reparation and further degenerative processes can be the ultimate outcome.
引用
收藏
页码：13 / 18
页数：6
相关论文
共 50 条
  • [21] Neuroprotection by D-securinine against neurotoxicity induced by beta-amyloid (25-35)
    Xu, L
    Zhang, JT
    NEUROLOGICAL RESEARCH, 2004, 26 (07) : 792 - 796
  • [22] Oxidative stress after acute and chronic application of beta-amyloid fragment 25-35 in cortical cultures
    Cafe, C
    Torri, C
    Bertorelli, L
    Angeretti, N
    Lucca, E
    Forloni, G
    Marzatico, F
    NEUROSCIENCE LETTERS, 1996, 203 (01) : 61 - 65
  • [23] INHIBITION OF GLUTAMATE TRANSPORTER BY 25-35 BETA-AMYLOID PROTEIN-FRAGMENT IN HUMAN RETINOBLASTOMA CELL
    CROSSON, CE
    GANEL, R
    ITTAH, A
    JOURNAL OF CELLULAR BIOCHEMISTRY, 1995, : 102 - 102
  • [24] Lentiviral-mediated overexpression of nerve growth factor (NGF) prevents beta-amyloid [25-35]-induced long term potentiation (LTP) decline in the rat hippocampus
    Uzakov, Shukhrat S.
    Ivanov, Andrey D.
    Salozhin, Sergey V.
    Markevich, Vladimir A.
    Gulyaeva, Natalia V.
    BRAIN RESEARCH, 2015, 1624 : 398 - 404
  • [25] Standardized extract of Centella asiatica ECa 233 improved cognitive deficits induced by beta-amyloid peptide (25-35)
    Tantisira, Mayuree H.
    Kam-Eg, Anchalee
    Tantisira, Boonyong
    JOURNAL OF PHARMACOLOGICAL SCIENCES, 2011, 115 : 91P - 91P
  • [26] Mechanisms underlying the vascular activity of beta-amyloid protein fragment (beta A(4)25-35) at the level of skin microvasculature
    Khalil, Z
    Chen, HB
    Helme, RD
    BRAIN RESEARCH, 1996, 736 (1-2) : 206 - 216
  • [27] AMYLOID BETA-PROTEIN FRAGMENT 25-35 CAUSES ACTIVATION OF CYTOPLASMIC CALCIUM IN NEURONS
    JOSEPH, R
    HAN, E
    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1992, 184 (03) : 1441 - 1447
  • [28] Administration of Aggregated Beta-Amyloid Peptide (25–35) Induces Changes in Long-Term Potentiation in the Hippocampus in Vivo
    V. V. Trubetskaya
    M. Yu. Stepanichev
    M. V. Onufriev
    N. A. Lazareva
    V. A. Markevich
    N. V. Gulyaeva
    Neuroscience and Behavioral Physiology, 2003, 33 (2) : 95 - 98
  • [29] Cytotoxicity of beta-amyloid peptide 25-35 on vascular smooth muscle cells and attenuation by vitamin E
    Gwebu, ET
    Williams, J
    Mathis, D
    Warden, JA
    Selassie, M
    Richardson, S
    Gwebu, NT
    IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL, 1997, 33 (09) : 672 - 673
  • [30] THE TROPHIC EFFECT OF BETA-AMYLOID 25-35 PEPTIDE IS NOT MEDIATED BY NK1 OR BOMBESIN RECEPTORS
    BURGEVIN, MC
    DANIEL, N
    DOBLE, A
    BLANCHARD, JC
    NEUROREPORT, 1992, 3 (12) : 1131 - 1134
12345