Targets for future clinical trials in Huntington's disease: what's in the pipeline?
Identifieur interne : 000411 ( PubMed/Corpus ); précédent : 000410; suivant : 000412Targets for future clinical trials in Huntington's disease: what's in the pipeline?
Auteurs : Edward J. Wild ; Sarah J. TabriziSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2014.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Histone Deacetylases, Nerve Tissue Proteins.
- genetics : Huntington Disease.
- chemical , metabolism : Nerve Tissue Proteins.
- methods : Clinical Trials as Topic, Genetic Therapy.
- therapy : Huntington Disease.
- trends : Clinical Trials as Topic.
- Animals, Gene Silencing, Humans.
Abstract
The known genetic cause of Huntington's disease (HD) has fueled considerable progress in understanding its pathobiology and the development of therapeutic approaches aimed at correcting specific changes linked to the causative mutation. Among the most promising is reducing expression of mutant huntingtin protein (mHTT) with RNA interference or antisense oligonucleotides; human trials are now being planned. Zinc-finger transcriptional repression is another innovative method to reduce mHTT expression. Modulation of mHTT phosphorylation, chaperone upregulation, and autophagy enhancement represent attempts to alter cellular homeostasis to favor removal of mHTT. Inhibition of histone deacetylases (HDACs) remains of interest; recent work affirms HDAC4 as a target but questions the assumed centrality of its catalytic activity in HD. Phosphodiesterase inhibition, aimed at restoring synaptic function, has progressed rapidly to human trials. Deranged cellular signaling provides several tractable targets, but specificity and complexity are challenges. Restoring neurotrophic support in HD remains a key potential therapeutic approach. with several approaches being pursued, including brain-derived neurotrophic factor (BDNF) mimesis through tyrosine receptor kinase B (TrkB) agonism and monoclonal antibodies. An increasing understanding of the role of glial cells in HD has led to several new therapeutic avenues, including kynurenine monooxygenase inhibition, immunomodulation by laquinimod, CB2 agonism, and others. The complex metabolic derangements in HD remain under study, but no clear therapeutic strategy has yet emerged. We conclude that many exciting therapeutics are progressing through the development pipeline, and combining a better understanding of HD biology in human patients, with concerted medicinal chemistry efforts, will be crucial for bringing about an era of effective therapies.
DOI: 10.1002/mds.26007
PubMed: 25155142
Links to Exploration step
pubmed:25155142Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Targets for future clinical trials in Huntington's disease: what's in the pipeline?</title><author><name sortKey="Wild, Edward J" sort="Wild, Edward J" uniqKey="Wild E" first="Edward J" last="Wild">Edward J. Wild</name><affiliation><nlm:affiliation>Department of Neurodegenerative Disease, UCL Institute of Neurology, National Hospital for Neurology & Neurosurgery, Queen Square, London, WC1N 3BG, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Tabrizi, Sarah J" sort="Tabrizi, Sarah J" uniqKey="Tabrizi S" first="Sarah J" last="Tabrizi">Sarah J. Tabrizi</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25155142</idno><idno type="pmid">25155142</idno><idno type="doi">10.1002/mds.26007</idno><idno type="wicri:Area/PubMed/Corpus">000411</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Targets for future clinical trials in Huntington's disease: what's in the pipeline?</title><author><name sortKey="Wild, Edward J" sort="Wild, Edward J" uniqKey="Wild E" first="Edward J" last="Wild">Edward J. Wild</name><affiliation><nlm:affiliation>Department of Neurodegenerative Disease, UCL Institute of Neurology, National Hospital for Neurology & Neurosurgery, Queen Square, London, WC1N 3BG, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Tabrizi, Sarah J" sort="Tabrizi, Sarah J" uniqKey="Tabrizi S" first="Sarah J" last="Tabrizi">Sarah J. Tabrizi</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Clinical Trials as Topic (methods)</term><term>Clinical Trials as Topic (trends)</term><term>Gene Silencing</term><term>Genetic Therapy (methods)</term><term>Histone Deacetylases (genetics)</term><term>Humans</term><term>Huntington Disease (genetics)</term><term>Huntington Disease (therapy)</term><term>Nerve Tissue Proteins (genetics)</term><term>Nerve Tissue Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Histone Deacetylases</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Clinical Trials as Topic</term><term>Genetic Therapy</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" qualifier="trends" xml:lang="en"><term>Clinical Trials as Topic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Silencing</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The known genetic cause of Huntington's disease (HD) has fueled considerable progress in understanding its pathobiology and the development of therapeutic approaches aimed at correcting specific changes linked to the causative mutation. Among the most promising is reducing expression of mutant huntingtin protein (mHTT) with RNA interference or antisense oligonucleotides; human trials are now being planned. Zinc-finger transcriptional repression is another innovative method to reduce mHTT expression. Modulation of mHTT phosphorylation, chaperone upregulation, and autophagy enhancement represent attempts to alter cellular homeostasis to favor removal of mHTT. Inhibition of histone deacetylases (HDACs) remains of interest; recent work affirms HDAC4 as a target but questions the assumed centrality of its catalytic activity in HD. Phosphodiesterase inhibition, aimed at restoring synaptic function, has progressed rapidly to human trials. Deranged cellular signaling provides several tractable targets, but specificity and complexity are challenges. Restoring neurotrophic support in HD remains a key potential therapeutic approach. with several approaches being pursued, including brain-derived neurotrophic factor (BDNF) mimesis through tyrosine receptor kinase B (TrkB) agonism and monoclonal antibodies. An increasing understanding of the role of glial cells in HD has led to several new therapeutic avenues, including kynurenine monooxygenase inhibition, immunomodulation by laquinimod, CB2 agonism, and others. The complex metabolic derangements in HD remain under study, but no clear therapeutic strategy has yet emerged. We conclude that many exciting therapeutics are progressing through the development pipeline, and combining a better understanding of HD biology in human patients, with concerted medicinal chemistry efforts, will be crucial for bringing about an era of effective therapies.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">25155142</PMID><DateCreated><Year>2014</Year><Month>09</Month><Day>13</Day></DateCreated><DateCompleted><Year>2015</Year><Month>05</Month><Day>15</Day></DateCompleted><DateRevised><Year>2015</Year><Month>07</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>11</Issue><PubDate><Year>2014</Year><Month>Sep</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Targets for future clinical trials in Huntington's disease: what's in the pipeline?</ArticleTitle><Pagination><MedlinePgn>1434-45</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.26007</ELocationID><Abstract><AbstractText>The known genetic cause of Huntington's disease (HD) has fueled considerable progress in understanding its pathobiology and the development of therapeutic approaches aimed at correcting specific changes linked to the causative mutation. Among the most promising is reducing expression of mutant huntingtin protein (mHTT) with RNA interference or antisense oligonucleotides; human trials are now being planned. Zinc-finger transcriptional repression is another innovative method to reduce mHTT expression. Modulation of mHTT phosphorylation, chaperone upregulation, and autophagy enhancement represent attempts to alter cellular homeostasis to favor removal of mHTT. Inhibition of histone deacetylases (HDACs) remains of interest; recent work affirms HDAC4 as a target but questions the assumed centrality of its catalytic activity in HD. Phosphodiesterase inhibition, aimed at restoring synaptic function, has progressed rapidly to human trials. Deranged cellular signaling provides several tractable targets, but specificity and complexity are challenges. Restoring neurotrophic support in HD remains a key potential therapeutic approach. with several approaches being pursued, including brain-derived neurotrophic factor (BDNF) mimesis through tyrosine receptor kinase B (TrkB) agonism and monoclonal antibodies. An increasing understanding of the role of glial cells in HD has led to several new therapeutic avenues, including kynurenine monooxygenase inhibition, immunomodulation by laquinimod, CB2 agonism, and others. The complex metabolic derangements in HD remain under study, but no clear therapeutic strategy has yet emerged. We conclude that many exciting therapeutics are progressing through the development pipeline, and combining a better understanding of HD biology in human patients, with concerted medicinal chemistry efforts, will be crucial for bringing about an era of effective therapies.</AbstractText><CopyrightInformation>© 2014 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wild</LastName><ForeName>Edward J</ForeName><Initials>EJ</Initials><AffiliationInfo><Affiliation>Department of Neurodegenerative Disease, UCL Institute of Neurology, National Hospital for Neurology & Neurosurgery, Queen Square, London, WC1N 3BG, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tabrizi</LastName><ForeName>Sarah J</ForeName><Initials>SJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>08</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C086055">HTT protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.5.1.98</RegistryNumber><NameOfSubstance UI="D006655">Histone Deacetylases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>N Engl J Med. 2012 Nov;367(18):1753-4</RefSource><PMID Version="1">23113488</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2012 Nov 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Mar;22(3):487-97</RefSource><PMID Version="1">24356252</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002986">Clinical Trials as Topic</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000379">methods</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000639">trends</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020868">Gene Silencing</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015316">Genetic Therapy</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006655">Histone Deacetylases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006816">Huntington Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000628">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009419">Nerve Tissue Proteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4265300</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">HDAC inhibition</Keyword><Keyword MajorTopicYN="N">Huntington's disease</Keyword><Keyword MajorTopicYN="N">MAPK</Keyword><Keyword MajorTopicYN="N">gene silencing</Keyword><Keyword MajorTopicYN="N">glial cells</Keyword><Keyword MajorTopicYN="N">kynurenine monooxygenase</Keyword><Keyword MajorTopicYN="N">phosphodiesterase inhibition</Keyword><Keyword MajorTopicYN="N">therapeutics</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>7</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>7</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>7</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2014</Year><Month>8</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>8</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>8</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>5</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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