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Article

Neuroprotective Effects of Tripeptides—Epigenetic Regulators in Mouse Model of Alzheimer’s Disease

1
Saint Petersburg Institute of Bioregulation and Gerontology, 197110 Saint Petersburg, Russia
2
Pavlov Institute of Physiology of Russian Academy of Sciences, 199034 Saint Petersburg, Russia
3
Institute of Biomedical Systems and Biotechnology, Peter the Great St. Petersburg State Polytechnic University, 195251 Saint Petersburg, Russia
4
Petersburg Nuclear Physics Institute Named after B.P. Konstantinov, NRC “Kurchatov Institute”, 188300 Gatchina, Russia
5
Russian Scientific Center of Radiology and Surgical Technologies Named after A.M. Granov, 197758 Saint Petersburg, Russia
*
Author to whom correspondence should be addressed.
Academic Editor: Marcin Ratajewski
Pharmaceuticals 2021, 14(6), 515; https://doi.org/10.3390/ph14060515
Received: 21 April 2021 / Revised: 19 May 2021 / Accepted: 26 May 2021 / Published: 27 May 2021
(This article belongs to the Special Issue Epigenetic Drugs)
KED and EDR peptides prevent dendritic spines loss in amyloid synaptotoxicity in in vitro model of Alzheimer’s disease (AD). The objective of this paper was to study epigenetic mechanisms of EDR and KED peptides’ neuroprotective effects on neuroplasticity and dendritic spine morphology in an AD mouse model. Daily intraperitoneal administration of the KED peptide in 5xFAD mice from 2 to 4 months of age at a concentration of 400 μg/kg tended to increase neuroplasticity. KED and EDR peptides prevented dendritic spine loss in 5xFAD-M mice. Their action’s possible molecular mechanisms were investigated by molecular modeling and docking of peptides in dsDNA, containing all possible combinations of hexanucleotide sequences. Similar DNA sequences were found in the lowest-energy complexes of the studied peptides with DNA in the classical B-form. EDR peptide has binding sites in the promoter region of CASP3, NES, GAP43, APOE, SOD2, PPARA, PPARG, GDX1 genes. Protein products of these genes are involved in AD pathogenesis. The neuroprotective effect of EDR and KED peptides in AD can be defined by their ability to prevent dendritic spine elimination and neuroplasticity impairments at the molecular epigenetic level. View Full-Text
Keywords: EDR peptide; KED peptide; epigenetic regulation; Alzheimer’s disease; gender; neuronal dendritic spines; neuroplasticity; 5xFAD mice EDR peptide; KED peptide; epigenetic regulation; Alzheimer’s disease; gender; neuronal dendritic spines; neuroplasticity; 5xFAD mice
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MDPI and ACS Style

Khavinson, V.; Ilina, A.; Kraskovskaya, N.; Linkova, N.; Kolchina, N.; Mironova, E.; Erofeev, A.; Petukhov, M. Neuroprotective Effects of Tripeptides—Epigenetic Regulators in Mouse Model of Alzheimer’s Disease. Pharmaceuticals 2021, 14, 515. https://doi.org/10.3390/ph14060515

AMA Style

Khavinson V, Ilina A, Kraskovskaya N, Linkova N, Kolchina N, Mironova E, Erofeev A, Petukhov M. Neuroprotective Effects of Tripeptides—Epigenetic Regulators in Mouse Model of Alzheimer’s Disease. Pharmaceuticals. 2021; 14(6):515. https://doi.org/10.3390/ph14060515

Chicago/Turabian Style

Khavinson, Vladimir, Anastasiia Ilina, Nina Kraskovskaya, Natalia Linkova, Nina Kolchina, Ekaterina Mironova, Alexander Erofeev, and Michael Petukhov. 2021. "Neuroprotective Effects of Tripeptides—Epigenetic Regulators in Mouse Model of Alzheimer’s Disease" Pharmaceuticals 14, no. 6: 515. https://doi.org/10.3390/ph14060515

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