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Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis
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Zeitschriftentitel: | British Journal of Pharmacology |
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Personen und Körperschaften: | , , |
In: | British Journal of Pharmacology, 178, 2021, 6, S. 1353-1372 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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Schlagwörter: |
author_facet |
Klingl, Yvonne E. Pakravan, Donya Van Den Bosch, Ludo Klingl, Yvonne E. Pakravan, Donya Van Den Bosch, Ludo |
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author |
Klingl, Yvonne E. Pakravan, Donya Van Den Bosch, Ludo |
spellingShingle |
Klingl, Yvonne E. Pakravan, Donya Van Den Bosch, Ludo British Journal of Pharmacology Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis Pharmacology |
author_sort |
klingl, yvonne e. |
spelling |
Klingl, Yvonne E. Pakravan, Donya Van Den Bosch, Ludo 0007-1188 1476-5381 Wiley Pharmacology http://dx.doi.org/10.1111/bph.15217 <jats:sec><jats:label /><jats:p>Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease. ALS patients suffer from a progressive loss of motor neurons, leading to respiratory failure within 3 to 5 years after diagnosis. Available therapies only slow down the disease progression moderately or extend the lifespan by a few months. Epigenetic hallmarks have been linked to the disease, creating an avenue for potential therapeutic approaches. Interference with one class of epigenetic enzymes, histone deacetylases, has been shown to affect neurodegeneration in many preclinical models. Consequently, it is crucial to improve our understanding about histone deacetylases and their inhibitors in (pre)clinical models of ALS. We conclude that selective inhibitors with high tolerability and safety and sufficient blood–brain barrier permeability will be needed to interfere with both epigenetic and non‐epigenetic targets of these enzymes.</jats:p></jats:sec><jats:sec><jats:title>LINKED ARTICLES</jats:title><jats:p>This article is part of a themed issue on Recent advances in ALS pathogenesis and therapeutics. To view the other articles in this section visit <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc">http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc</jats:ext-link></jats:p></jats:sec> Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis British Journal of Pharmacology |
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title |
Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_unstemmed |
Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_full |
Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_fullStr |
Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_full_unstemmed |
Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_short |
Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_sort |
opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
topic |
Pharmacology |
url |
http://dx.doi.org/10.1111/bph.15217 |
publishDate |
2021 |
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<jats:sec><jats:label /><jats:p>Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease. ALS patients suffer from a progressive loss of motor neurons, leading to respiratory failure within 3 to 5 years after diagnosis. Available therapies only slow down the disease progression moderately or extend the lifespan by a few months. Epigenetic hallmarks have been linked to the disease, creating an avenue for potential therapeutic approaches. Interference with one class of epigenetic enzymes, histone deacetylases, has been shown to affect neurodegeneration in many preclinical models. Consequently, it is crucial to improve our understanding about histone deacetylases and their inhibitors in (pre)clinical models of ALS. We conclude that selective inhibitors with high tolerability and safety and sufficient blood–brain barrier permeability will be needed to interfere with both epigenetic and non‐epigenetic targets of these enzymes.</jats:p></jats:sec><jats:sec><jats:title>LINKED ARTICLES</jats:title><jats:p>This article is part of a themed issue on Recent advances in ALS pathogenesis and therapeutics. To view the other articles in this section visit <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc">http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc</jats:ext-link></jats:p></jats:sec> |
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author | Klingl, Yvonne E., Pakravan, Donya, Van Den Bosch, Ludo |
author_facet | Klingl, Yvonne E., Pakravan, Donya, Van Den Bosch, Ludo, Klingl, Yvonne E., Pakravan, Donya, Van Den Bosch, Ludo |
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description | <jats:sec><jats:label /><jats:p>Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease. ALS patients suffer from a progressive loss of motor neurons, leading to respiratory failure within 3 to 5 years after diagnosis. Available therapies only slow down the disease progression moderately or extend the lifespan by a few months. Epigenetic hallmarks have been linked to the disease, creating an avenue for potential therapeutic approaches. Interference with one class of epigenetic enzymes, histone deacetylases, has been shown to affect neurodegeneration in many preclinical models. Consequently, it is crucial to improve our understanding about histone deacetylases and their inhibitors in (pre)clinical models of ALS. We conclude that selective inhibitors with high tolerability and safety and sufficient blood–brain barrier permeability will be needed to interfere with both epigenetic and non‐epigenetic targets of these enzymes.</jats:p></jats:sec><jats:sec><jats:title>LINKED ARTICLES</jats:title><jats:p>This article is part of a themed issue on Recent advances in ALS pathogenesis and therapeutics. To view the other articles in this section visit <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc">http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc</jats:ext-link></jats:p></jats:sec> |
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spelling | Klingl, Yvonne E. Pakravan, Donya Van Den Bosch, Ludo 0007-1188 1476-5381 Wiley Pharmacology http://dx.doi.org/10.1111/bph.15217 <jats:sec><jats:label /><jats:p>Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease. ALS patients suffer from a progressive loss of motor neurons, leading to respiratory failure within 3 to 5 years after diagnosis. Available therapies only slow down the disease progression moderately or extend the lifespan by a few months. Epigenetic hallmarks have been linked to the disease, creating an avenue for potential therapeutic approaches. Interference with one class of epigenetic enzymes, histone deacetylases, has been shown to affect neurodegeneration in many preclinical models. Consequently, it is crucial to improve our understanding about histone deacetylases and their inhibitors in (pre)clinical models of ALS. We conclude that selective inhibitors with high tolerability and safety and sufficient blood–brain barrier permeability will be needed to interfere with both epigenetic and non‐epigenetic targets of these enzymes.</jats:p></jats:sec><jats:sec><jats:title>LINKED ARTICLES</jats:title><jats:p>This article is part of a themed issue on Recent advances in ALS pathogenesis and therapeutics. To view the other articles in this section visit <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc">http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc</jats:ext-link></jats:p></jats:sec> Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis British Journal of Pharmacology |
spellingShingle | Klingl, Yvonne E., Pakravan, Donya, Van Den Bosch, Ludo, British Journal of Pharmacology, Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis, Pharmacology |
title | Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_full | Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_fullStr | Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_full_unstemmed | Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_short | Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_sort | opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
title_unstemmed | Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis |
topic | Pharmacology |
url | http://dx.doi.org/10.1111/bph.15217 |