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Histone Modifications in Alzheimer’s Disease

Since Late-onset Alzheimer’s disease (LOAD) derives from a combination of genetic variants and environmental factors, epigenetic modifications have been predicted to play a role in the etiopathology of LOAD. Along with DNA methylation, histone modifications have been proposed as the main epigenetic...

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Autores principales: Santana, Dalileia Aparecida, Smith, Marilia de Arruda Cardoso, Chen, Elizabeth Suchi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9956192/
https://www.ncbi.nlm.nih.gov/pubmed/36833274
http://dx.doi.org/10.3390/genes14020347
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author Santana, Dalileia Aparecida
Smith, Marilia de Arruda Cardoso
Chen, Elizabeth Suchi
author_facet Santana, Dalileia Aparecida
Smith, Marilia de Arruda Cardoso
Chen, Elizabeth Suchi
author_sort Santana, Dalileia Aparecida
collection PubMed
description Since Late-onset Alzheimer’s disease (LOAD) derives from a combination of genetic variants and environmental factors, epigenetic modifications have been predicted to play a role in the etiopathology of LOAD. Along with DNA methylation, histone modifications have been proposed as the main epigenetic modifications that contribute to the pathologic mechanisms of LOAD; however, little is known about how these mechanisms contribute to the disease’s onset or progression. In this review, we highlighted the main histone modifications and their functional role, including histone acetylation, histone methylation, and histone phosphorylation, as well as changes in such histone modifications that occur in the aging process and mainly in Alzheimer’s disease (AD). Furthermore, we pointed out the main epigenetic drugs tested for AD treatment, such as those based on histone deacetylase (HDAC) inhibitors. Finally, we remarked on the perspectives around the use of such epigenetics drugs for treating AD.
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spelling pubmed-99561922023-02-25 Histone Modifications in Alzheimer’s Disease Santana, Dalileia Aparecida Smith, Marilia de Arruda Cardoso Chen, Elizabeth Suchi Genes (Basel) Review Since Late-onset Alzheimer’s disease (LOAD) derives from a combination of genetic variants and environmental factors, epigenetic modifications have been predicted to play a role in the etiopathology of LOAD. Along with DNA methylation, histone modifications have been proposed as the main epigenetic modifications that contribute to the pathologic mechanisms of LOAD; however, little is known about how these mechanisms contribute to the disease’s onset or progression. In this review, we highlighted the main histone modifications and their functional role, including histone acetylation, histone methylation, and histone phosphorylation, as well as changes in such histone modifications that occur in the aging process and mainly in Alzheimer’s disease (AD). Furthermore, we pointed out the main epigenetic drugs tested for AD treatment, such as those based on histone deacetylase (HDAC) inhibitors. Finally, we remarked on the perspectives around the use of such epigenetics drugs for treating AD. MDPI 2023-01-29 /pmc/articles/PMC9956192/ /pubmed/36833274 http://dx.doi.org/10.3390/genes14020347 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Santana, Dalileia Aparecida
Smith, Marilia de Arruda Cardoso
Chen, Elizabeth Suchi
Histone Modifications in Alzheimer’s Disease
title Histone Modifications in Alzheimer’s Disease
title_full Histone Modifications in Alzheimer’s Disease
title_fullStr Histone Modifications in Alzheimer’s Disease
title_full_unstemmed Histone Modifications in Alzheimer’s Disease
title_short Histone Modifications in Alzheimer’s Disease
title_sort histone modifications in alzheimer’s disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9956192/
https://www.ncbi.nlm.nih.gov/pubmed/36833274
http://dx.doi.org/10.3390/genes14020347
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