Targeting epigenetics: A novel promise for Alzheimer’s disease treatment
So far, the search for a cure for Alzheimer Disease (AD) has been unsuccessful. The only approved drugs attenuate some symptoms, but do not halt the progress of this disease, which affects 50 million people worldwide and will increase its incidence in the coming decades. Such scenario demands new th...
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Published in | Ageing research reviews Vol. 90; p. 102003 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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Elsevier B.V
01.09.2023
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Abstract | So far, the search for a cure for Alzheimer Disease (AD) has been unsuccessful. The only approved drugs attenuate some symptoms, but do not halt the progress of this disease, which affects 50 million people worldwide and will increase its incidence in the coming decades. Such scenario demands new therapeutic approaches to fight against this devastating dementia. In recent years, multi-omics research and the analysis of differential epigenetic marks in AD subjects have contributed to our understanding of AD; however, the impact of epigenetic research is yet to be seen. This review integrates the most recent data on pathological processes and epigenetic changes relevant for aging and AD, as well as current therapies targeting epigenetic machinery in clinical trials. Evidence shows that epigenetic modifications play a key role in gene expression, which could provide multi-target preventative and therapeutic approaches in AD. Both novel and repurposed drugs are employed in AD clinical trials due to their epigenetic effects, as well as increasing number of natural compounds. Given the reversible nature of epigenetic modifications and the complexity of gene-environment interactions, the combination of epigenetic-based therapies with environmental strategies and drugs with multiple targets might be needed to properly help AD patients.
•Epigenetic studies provided numerous data on the role of gene expression changes in AD.•Studies tend to be neuron-centric focused on DNA methylation, histone modification and non-coding RNAs.•Epigenetic should be incorporated in molecular etiology of AD at different levels of biological complexity•Preventative strategies against AD epigenetic factors ought to integrate with future multi-target therapies. |
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AbstractList | So far, the search for a cure for Alzheimer Disease (AD) has been unsuccessful. The only approved drugs attenuate some symptoms, but do not halt the progress of this disease, which affects 50 million people worldwide and will increase its incidence in the coming decades. Such scenario demands new therapeutic approaches to fight against this devastating dementia. In recent years, multi-omics research and the analysis of differential epigenetic marks in AD subjects have contributed to our understanding of AD; however, the impact of epigenetic research is yet to be seen. This review integrates the most recent data on pathological processes and epigenetic changes relevant for aging and AD, as well as current therapies targeting epigenetic machinery in clinical trials. Evidence shows that epigenetic modifications play a key role in gene expression, which could provide multi-target preventative and therapeutic approaches in AD. Both novel and repurposed drugs are employed in AD clinical trials due to their epigenetic effects, as well as increasing number of natural compounds. Given the reversible nature of epigenetic modifications and the complexity of gene-environment interactions, the combination of epigenetic-based therapies with environmental strategies and drugs with multiple targets might be needed to properly help AD patients.
•Epigenetic studies provided numerous data on the role of gene expression changes in AD.•Studies tend to be neuron-centric focused on DNA methylation, histone modification and non-coding RNAs.•Epigenetic should be incorporated in molecular etiology of AD at different levels of biological complexity•Preventative strategies against AD epigenetic factors ought to integrate with future multi-target therapies. So far, the search for a cure for Alzheimer Disease (AD) has been unsuccessful. The only approved drugs attenuate some symptoms, but do not halt the progress of this disease, which affects 50 million people worldwide and will increase its incidence in the coming decades. Such scenario demands new therapeutic approaches to fight against this devastating dementia. In recent years, multi-omics research and the analysis of differential epigenetic marks in AD subjects have contributed to our understanding of AD; however, the impact of epigenetic research is yet to be seen. This review integrates the most recent data on pathological processes and epigenetic changes relevant for aging and AD, as well as current therapies targeting epigenetic machinery in clinical trials. Evidence shows that epigenetic modifications play a key role in gene expression, which could provide multi-target preventative and therapeutic approaches in AD. Both novel and repurposed drugs are employed in AD clinical trials due to their epigenetic effects, as well as increasing number of natural compounds. Given the reversible nature of epigenetic modifications and the complexity of gene-environment interactions, the combination of epigenetic-based therapies with environmental strategies and drugs with multiple targets might be needed to properly help AD patients.So far, the search for a cure for Alzheimer Disease (AD) has been unsuccessful. The only approved drugs attenuate some symptoms, but do not halt the progress of this disease, which affects 50 million people worldwide and will increase its incidence in the coming decades. Such scenario demands new therapeutic approaches to fight against this devastating dementia. In recent years, multi-omics research and the analysis of differential epigenetic marks in AD subjects have contributed to our understanding of AD; however, the impact of epigenetic research is yet to be seen. This review integrates the most recent data on pathological processes and epigenetic changes relevant for aging and AD, as well as current therapies targeting epigenetic machinery in clinical trials. Evidence shows that epigenetic modifications play a key role in gene expression, which could provide multi-target preventative and therapeutic approaches in AD. Both novel and repurposed drugs are employed in AD clinical trials due to their epigenetic effects, as well as increasing number of natural compounds. Given the reversible nature of epigenetic modifications and the complexity of gene-environment interactions, the combination of epigenetic-based therapies with environmental strategies and drugs with multiple targets might be needed to properly help AD patients. So far, the search for a cure for Alzheimer Disease (AD) has been unsuccessful. The only approved drugs attenuate some symptoms, but do not halt the progress of this disease, which affects 50 million people worldwide and will increase its incidence in the coming decades. Such scenario demands new therapeutic approaches to fight against this devastating dementia. In recent years, multi-omics research and the analysis of differential epigenetic marks in AD subjects have contributed to our understanding of AD; however, the impact of epigenetic research is yet to be seen. This review integrates the most recent data on pathological processes and epigenetic changes relevant for aging and AD, as well as current therapies targeting epigenetic machinery in clinical trials. Evidence shows that epigenetic modifications play a key role in gene expression, which could provide multi-target preventative and therapeutic approaches in AD. Both novel and repurposed drugs are employed in AD clinical trials due to their epigenetic effects, as well as increasing number of natural compounds. Given the reversible nature of epigenetic modifications and the complexity of gene-environment interactions, the combination of epigenetic-based therapies with environmental strategies and drugs with multiple targets might be needed to properly help AD patients. |
ArticleNumber | 102003 |
Author | Jeremic, Danko Navarro-López, Juan D. Jiménez-Díaz, Lydia |
Author_xml | – sequence: 1 givenname: Danko surname: Jeremic fullname: Jeremic, Danko – sequence: 2 givenname: Lydia surname: Jiménez-Díaz fullname: Jiménez-Díaz, Lydia email: Lydia.Jimenez@uclm.es – sequence: 3 givenname: Juan D. surname: Navarro-López fullname: Navarro-López, Juan D. email: Juan.Navarro@uclm.es |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37422087$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1080_01932691_2024_2434704 crossref_primary_10_3389_fnut_2024_1483790 crossref_primary_10_3390_life14121555 crossref_primary_10_1021_acsomega_3c07046 crossref_primary_10_1038_s41392_024_02095_6 crossref_primary_10_3390_nu16091288 crossref_primary_10_1007_s00580_024_03603_4 crossref_primary_10_1177_20552173241296726 crossref_primary_10_1021_acs_jmedchem_4c03049 crossref_primary_10_1016_j_sleep_2024_05_010 crossref_primary_10_3389_fnagi_2024_1332845 crossref_primary_10_1016_j_arr_2024_102267 crossref_primary_10_4103_1673_5374_391335 crossref_primary_10_1016_j_inoche_2024_113843 crossref_primary_10_1186_s12967_023_04749_5 |
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