Heat shock proteins as potential targets for protective strategies in neurodegeneration
Summary Protein aggregates are hallmarks of nearly all age-related neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and several polyglutamine diseases such as Huntington's disease and different forms of spinocerebellar atax...
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| Veröffentlicht in: | Lancet neurology 2016-06, Vol.15 (7), p.748-759 |
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| creator | Kampinga, Harm H, Prof Bergink, Steven, PhD |
| description | Summary Protein aggregates are hallmarks of nearly all age-related neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and several polyglutamine diseases such as Huntington's disease and different forms of spinocerebellar ataxias (SCA; SCA1–3, SCA6, and SCA7). The collapse of cellular protein homoeostasis can be both a cause and a consequence of this protein aggregation. Boosting components of the cellular protein quality control system has been widely investigated as a strategy to counteract protein aggregates or their toxic consequences. Heat shock proteins (HSPs) play a central part in regulating protein quality control and contribute to protein aggregation and disaggregation. Therefore, HSPs are viable targets for the development of drugs aimed at reducing pathogenic protein aggregates that are thought to contribute to the development of so many neurodegenerative disorders. |
| doi_str_mv | 10.1016/S1474-4422(16)00099-5 |
| format | Article |
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The collapse of cellular protein homoeostasis can be both a cause and a consequence of this protein aggregation. Boosting components of the cellular protein quality control system has been widely investigated as a strategy to counteract protein aggregates or their toxic consequences. Heat shock proteins (HSPs) play a central part in regulating protein quality control and contribute to protein aggregation and disaggregation. Therefore, HSPs are viable targets for the development of drugs aimed at reducing pathogenic protein aggregates that are thought to contribute to the development of so many neurodegenerative disorders.</description><identifier>ISSN: 1474-4422</identifier><identifier>EISSN: 1474-4465</identifier><identifier>DOI: 10.1016/S1474-4422(16)00099-5</identifier><identifier>PMID: 27106072</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Age ; Alzheimer's disease ; Amyotrophic lateral sclerosis ; Animals ; Heat shock proteins ; Heat-Shock Proteins - drug effects ; Heat-Shock Proteins - metabolism ; Humans ; Hypotheses ; Mutation ; Neurodegeneration ; Neurodegenerative Diseases - drug therapy ; Neurodegenerative Diseases - metabolism ; Neurology ; Parkinson's disease ; Pathology ; Propagation ; Protein folding ; Stress response ; Toxicity</subject><ispartof>Lancet neurology, 2016-06, Vol.15 (7), p.748-759</ispartof><rights>Elsevier Ltd</rights><rights>2016 Elsevier Ltd</rights><rights>Copyright © 2016 Elsevier Ltd. All rights reserved.</rights><rights>Copyright Elsevier Limited Jun 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c500t-66c40c435ff8cc203514a4b643287298095882a5cb7528c4298175913774740d3</citedby><cites>FETCH-LOGICAL-c500t-66c40c435ff8cc203514a4b643287298095882a5cb7528c4298175913774740d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1789504684?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27106072$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kampinga, Harm H, Prof</creatorcontrib><creatorcontrib>Bergink, Steven, PhD</creatorcontrib><title>Heat shock proteins as potential targets for protective strategies in neurodegeneration</title><title>Lancet neurology</title><addtitle>Lancet Neurol</addtitle><description>Summary Protein aggregates are hallmarks of nearly all age-related neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and several polyglutamine diseases such as Huntington's disease and different forms of spinocerebellar ataxias (SCA; SCA1–3, SCA6, and SCA7). The collapse of cellular protein homoeostasis can be both a cause and a consequence of this protein aggregation. Boosting components of the cellular protein quality control system has been widely investigated as a strategy to counteract protein aggregates or their toxic consequences. Heat shock proteins (HSPs) play a central part in regulating protein quality control and contribute to protein aggregation and disaggregation. Therefore, HSPs are viable targets for the development of drugs aimed at reducing pathogenic protein aggregates that are thought to contribute to the development of so many neurodegenerative disorders.</description><subject>Age</subject><subject>Alzheimer's disease</subject><subject>Amyotrophic lateral sclerosis</subject><subject>Animals</subject><subject>Heat shock proteins</subject><subject>Heat-Shock Proteins - drug effects</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Mutation</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative Diseases - drug therapy</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurology</subject><subject>Parkinson's disease</subject><subject>Pathology</subject><subject>Propagation</subject><subject>Protein folding</subject><subject>Stress response</subject><subject>Toxicity</subject><issn>1474-4422</issn><issn>1474-4465</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkE1v1DAQhi0EoqXwE0CRuJRDYOz4KxcqVNEWqRIHQBwtrzNZ3GbtxXYq9d_j3SxF6oWTx6PHr2ceQl5TeE-Byg_fKFe85ZyxUyrfAUDft-IJOT60pXj6UDN2RF7kfAPAKNf0OTliioIExY7Jzyu0pcm_ortttikW9CE3NjfbWobi7dQUm9ZYcjPGtBCu-Dtsckm24NpjbnxoAs4pDrjGgLXtY3hJno12yvjqcJ6QHxefv59ftddfL7-cf7punQAorZSOg-OdGEftHINOUG75SvKOacV6Db3QmlnhVkow7XhtUSV62ilVd4OhOyGnS24d7feMuZiNzw6nyQaMczZU9UpwSmlf0beP0Js4p1Cnq5TuBXCpeaXEQrkUc044mm3yG5vuDQWzM2_25s1Oq6m3vXkj6rs3h_R5tcHh4dVf1RU4WwCsOu48JpOdx-Bw8Kk6NUP0__3i46MEN_ngnZ1u8R7zv21MZgaWkF0GlfsE0f0BD06l0w</recordid><startdate>20160601</startdate><enddate>20160601</enddate><creator>Kampinga, Harm H, Prof</creator><creator>Bergink, Steven, PhD</creator><general>Elsevier Ltd</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0TZ</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8C2</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20160601</creationdate><title>Heat shock proteins as potential targets for protective strategies in neurodegeneration</title><author>Kampinga, Harm H, Prof ; Bergink, Steven, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c500t-66c40c435ff8cc203514a4b643287298095882a5cb7528c4298175913774740d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Age</topic><topic>Alzheimer's disease</topic><topic>Amyotrophic lateral sclerosis</topic><topic>Animals</topic><topic>Heat shock proteins</topic><topic>Heat-Shock Proteins - drug effects</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Mutation</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative Diseases - drug therapy</topic><topic>Neurodegenerative Diseases - metabolism</topic><topic>Neurology</topic><topic>Parkinson's disease</topic><topic>Pathology</topic><topic>Propagation</topic><topic>Protein folding</topic><topic>Stress response</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kampinga, Harm H, Prof</creatorcontrib><creatorcontrib>Bergink, Steven, PhD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Pharma and Biotech Premium PRO</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Lancet Titles</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Lancet neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kampinga, Harm H, Prof</au><au>Bergink, Steven, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heat shock proteins as potential targets for protective strategies in neurodegeneration</atitle><jtitle>Lancet neurology</jtitle><addtitle>Lancet Neurol</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>15</volume><issue>7</issue><spage>748</spage><epage>759</epage><pages>748-759</pages><issn>1474-4422</issn><eissn>1474-4465</eissn><coden>LANCAO</coden><abstract>Summary Protein aggregates are hallmarks of nearly all age-related neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and several polyglutamine diseases such as Huntington's disease and different forms of spinocerebellar ataxias (SCA; 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| subjects | Age Alzheimer's disease Amyotrophic lateral sclerosis Animals Heat shock proteins Heat-Shock Proteins - drug effects Heat-Shock Proteins - metabolism Humans Hypotheses Mutation Neurodegeneration Neurodegenerative Diseases - drug therapy Neurodegenerative Diseases - metabolism Neurology Parkinson's disease Pathology Propagation Protein folding Stress response Toxicity |
| title | Heat shock proteins as potential targets for protective strategies in neurodegeneration |
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