ORIGINAL RESEARCH
Neurodegenerative changes induced by injection of β-amyloid peptide fragment (25-35) in hippocampus are associated with NGF-signalling activation
Functional Biochemistry of Nervous System Laboratory,Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia
Correspondence should be addressed: Mikhail Stepanichev
ul. Butlerova, d. 5А, Moscow, Russia, 117485; moc.oohay@vehcinapets_liahkim
Funding: this study was supported by the Russian Foundation for Basic Research (grants no. 13-04-01019a and 16-04-01054a ).
β-amyloid peptide (Аβ) is an important component of the neurodegeneration mechanism in Alzheimer’s disease. This work investigates the effect of intrahippocampal injection of Аβ(25–35) fragment on nerve growth factor (NGF) signalling. Aggregated Аβ(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 Аβ(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 Аβ(25–35). The study results demonstrate that changes in the hippocampus induced by Аβ(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.
Keywords: Alzheimer’s disease, β-amyloid peptide, hippocampus, nerve growth factor, p75NTR receptor, neurodegeneration