Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease
Epigenetic regulation of gene expression is necessary for maintaining higher-order cognitive functions (learning and memory). The current understanding of the role of epigenetics in the mechanism of Alzheimer’s disease (AD) is focused on DNA methylation, chromatin remodeling, histone modifications,...
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| Format: | Article |
| Language: | English |
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MDPI AG
2022-04-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/23/8/4259 |
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| author | Anastasiia Ilina Vladimir Khavinson Natalia Linkova Mikhael Petukhov |
| author_facet | Anastasiia Ilina Vladimir Khavinson Natalia Linkova Mikhael Petukhov |
| author_sort | Anastasiia Ilina |
| collection | DOAJ |
| description | Epigenetic regulation of gene expression is necessary for maintaining higher-order cognitive functions (learning and memory). The current understanding of the role of epigenetics in the mechanism of Alzheimer’s disease (AD) is focused on DNA methylation, chromatin remodeling, histone modifications, and regulation of non-coding RNAs. The pathogenetic links of this disease are the misfolding and aggregation of tau protein and amyloid peptides, mitochondrial dysfunction, oxidative stress, impaired energy metabolism, destruction of the blood–brain barrier, and neuroinflammation, all of which lead to impaired synaptic plasticity and memory loss. Ultrashort peptides are promising neuroprotective compounds with a broad spectrum of activity and without reported side effects. The main aim of this review is to analyze the possible epigenetic mechanisms of the neuroprotective action of ultrashort peptides in AD. The review highlights the role of short peptides in the AD pathophysiology. We formulate the hypothesis that peptide regulation of gene expression can be mediated by the interaction of short peptides with histone proteins, cis- and transregulatory DNA elements and effector molecules (DNA/RNA-binding proteins and non-coding RNA). The development of therapeutic agents based on ultrashort peptides may offer a promising addition to the multifunctional treatment of AD. |
| first_indexed | 2024-03-09T10:34:24Z |
| format | Article |
| id | doaj.art-aa1601083c17437291fca8711ca66e61 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T10:34:24Z |
| publishDate | 2022-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-aa1601083c17437291fca8711ca66e612023-12-01T21:03:28ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-04-01238425910.3390/ijms23084259Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s DiseaseAnastasiia Ilina0Vladimir Khavinson1Natalia Linkova2Mikhael Petukhov3Department of Biogerontology, Saint Petersburg Institute of Bioregulation and Gerontology, 19711 Saint Petersburg, RussiaDepartment of Biogerontology, Saint Petersburg Institute of Bioregulation and Gerontology, 19711 Saint Petersburg, RussiaDepartment of Biogerontology, Saint Petersburg Institute of Bioregulation and Gerontology, 19711 Saint Petersburg, RussiaDepartment of Molecular Radiation Biophysics, Petersburg Nuclear Physics Institute Named after B.P. Konstantinov, NRC “Kurchatov Institute”, 188300 Gatchina, RussiaEpigenetic regulation of gene expression is necessary for maintaining higher-order cognitive functions (learning and memory). The current understanding of the role of epigenetics in the mechanism of Alzheimer’s disease (AD) is focused on DNA methylation, chromatin remodeling, histone modifications, and regulation of non-coding RNAs. The pathogenetic links of this disease are the misfolding and aggregation of tau protein and amyloid peptides, mitochondrial dysfunction, oxidative stress, impaired energy metabolism, destruction of the blood–brain barrier, and neuroinflammation, all of which lead to impaired synaptic plasticity and memory loss. Ultrashort peptides are promising neuroprotective compounds with a broad spectrum of activity and without reported side effects. The main aim of this review is to analyze the possible epigenetic mechanisms of the neuroprotective action of ultrashort peptides in AD. The review highlights the role of short peptides in the AD pathophysiology. We formulate the hypothesis that peptide regulation of gene expression can be mediated by the interaction of short peptides with histone proteins, cis- and transregulatory DNA elements and effector molecules (DNA/RNA-binding proteins and non-coding RNA). The development of therapeutic agents based on ultrashort peptides may offer a promising addition to the multifunctional treatment of AD.https://www.mdpi.com/1422-0067/23/8/4259ultrashort peptidesDNApromotorshistonesnucleosomeDNA-binding proteins |
| spellingShingle | Anastasiia Ilina Vladimir Khavinson Natalia Linkova Mikhael Petukhov Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease International Journal of Molecular Sciences ultrashort peptides DNA promotors histones nucleosome DNA-binding proteins |
| title | Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease |
| title_full | Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease |
| title_fullStr | Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease |
| title_full_unstemmed | Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease |
| title_short | Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease |
| title_sort | neuroepigenetic mechanisms of action of ultrashort peptides in alzheimer s disease |
| topic | ultrashort peptides DNA promotors histones nucleosome DNA-binding proteins |
| url | https://www.mdpi.com/1422-0067/23/8/4259 |
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