Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease.
<h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have...
Ausführliche Beschreibung
Autor*in: |
Lesley Jones [verfasserIn] Peter A Holmans [verfasserIn] Marian L Hamshere [verfasserIn] Denise Harold [verfasserIn] Valentina Moskvina [verfasserIn] Dobril Ivanov [verfasserIn] Andrew Pocklington [verfasserIn] Richard Abraham [verfasserIn] Paul Hollingworth [verfasserIn] Rebecca Sims [verfasserIn] Amy Gerrish [verfasserIn] Jaspreet Singh Pahwa [verfasserIn] Nicola Jones [verfasserIn] Alexandra Stretton [verfasserIn] Angharad R Morgan [verfasserIn] Simon Lovestone [verfasserIn] John Powell [verfasserIn] Petroula Proitsi [verfasserIn] Michelle K Lupton [verfasserIn] Carol Brayne [verfasserIn] David C Rubinsztein [verfasserIn] Michael Gill [verfasserIn] Brian Lawlor [verfasserIn] Aoibhinn Lynch [verfasserIn] Kevin Morgan [verfasserIn] Kristelle S Brown [verfasserIn] Peter A Passmore [verfasserIn] David Craig [verfasserIn] Bernadette McGuinness [verfasserIn] Stephen Todd [verfasserIn] Clive Holmes [verfasserIn] David Mann [verfasserIn] A David Smith [verfasserIn] Seth Love [verfasserIn] Patrick G Kehoe [verfasserIn] Simon Mead [verfasserIn] Nick Fox [verfasserIn] Martin Rossor [verfasserIn] John Collinge [verfasserIn] Wolfgang Maier [verfasserIn] Frank Jessen [verfasserIn] Britta Schürmann [verfasserIn] Reinhard Heun [verfasserIn] Heike Kölsch [verfasserIn] Hendrik van den Bussche [verfasserIn] Isabella Heuser [verfasserIn] Oliver Peters [verfasserIn] Johannes Kornhuber [verfasserIn] Jens Wiltfang [verfasserIn] Martin Dichgans [verfasserIn] Lutz Frölich [verfasserIn] Harald Hampel [verfasserIn] Michael Hüll [verfasserIn] Dan Rujescu [verfasserIn] Alison M Goate [verfasserIn] John S K Kauwe [verfasserIn] Carlos Cruchaga [verfasserIn] Petra Nowotny [verfasserIn] John C Morris [verfasserIn] Kevin Mayo [verfasserIn] Gill Livingston [verfasserIn] Nicholas J Bass [verfasserIn] Hugh Gurling [verfasserIn] Andrew McQuillin [verfasserIn] Rhian Gwilliam [verfasserIn] Panos Deloukas [verfasserIn] Ammar Al-Chalabi [verfasserIn] Christopher E Shaw [verfasserIn] Andrew B Singleton [verfasserIn] Rita Guerreiro [verfasserIn] Thomas W Mühleisen [verfasserIn] Markus M Nöthen [verfasserIn] Susanne Moebus [verfasserIn] Karl-Heinz Jöckel [verfasserIn] Norman Klopp [verfasserIn] H-Erich Wichmann [verfasserIn] Eckhard Rüther [verfasserIn] Minerva M Carrasquillo [verfasserIn] V Shane Pankratz [verfasserIn] Steven G Younkin [verfasserIn] John Hardy [verfasserIn] Michael C O'Donovan [verfasserIn] Michael J Owen [verfasserIn] Julie Williams [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2010 |
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Übergeordnetes Werk: |
In: PLoS ONE - Public Library of Science (PLoS), 2007, 5(2010), 11, p e13950 |
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Übergeordnetes Werk: |
volume:5 ; year:2010 ; number:11, p e13950 |
Links: |
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DOI / URN: |
10.1371/journal.pone.0013950 |
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Katalog-ID: |
DOAJ046502181 |
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100 | 0 | |a Lesley Jones |e verfasserin |4 aut | |
245 | 1 | 0 | |a Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. |
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520 | |a <h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. | ||
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10.1371/journal.pone.0013950 doi (DE-627)DOAJ046502181 (DE-599)DOAJf60141a186cd4676b259fd600531e266 DE-627 ger DE-627 rakwb eng Lesley Jones verfasserin aut Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. Medicine R Science Q Peter A Holmans verfasserin aut Marian L Hamshere verfasserin aut Denise Harold verfasserin aut Valentina Moskvina verfasserin aut Dobril Ivanov verfasserin aut Andrew Pocklington verfasserin aut Richard Abraham verfasserin aut Paul Hollingworth verfasserin aut Rebecca Sims verfasserin aut Amy Gerrish verfasserin aut Jaspreet Singh Pahwa verfasserin aut Nicola Jones verfasserin aut Alexandra Stretton verfasserin aut Angharad R Morgan verfasserin aut Simon Lovestone verfasserin aut John Powell verfasserin aut Petroula Proitsi verfasserin aut Michelle K Lupton verfasserin aut Carol Brayne verfasserin aut David C Rubinsztein verfasserin aut Michael Gill verfasserin aut Brian Lawlor verfasserin aut Aoibhinn Lynch verfasserin aut Kevin Morgan verfasserin aut Kristelle S Brown verfasserin aut Peter A Passmore verfasserin aut David Craig verfasserin aut Bernadette McGuinness verfasserin aut Stephen Todd verfasserin aut Clive Holmes verfasserin aut David Mann verfasserin aut A David Smith verfasserin aut Seth Love verfasserin aut Patrick G Kehoe verfasserin aut Simon Mead verfasserin aut Nick Fox verfasserin aut Martin Rossor verfasserin aut John Collinge verfasserin aut Wolfgang Maier verfasserin aut Frank Jessen verfasserin aut Britta Schürmann verfasserin aut Reinhard Heun verfasserin aut Heike Kölsch verfasserin aut Hendrik van den Bussche verfasserin aut Isabella Heuser verfasserin aut Oliver Peters verfasserin aut Johannes Kornhuber verfasserin aut Jens Wiltfang verfasserin aut Martin Dichgans verfasserin aut Lutz Frölich verfasserin aut Harald Hampel verfasserin aut Michael Hüll verfasserin aut Dan Rujescu verfasserin aut Alison M Goate verfasserin aut John S K Kauwe verfasserin aut Carlos Cruchaga verfasserin aut Petra Nowotny verfasserin aut John C Morris verfasserin aut Kevin Mayo verfasserin aut Gill Livingston verfasserin aut Nicholas J Bass verfasserin aut Hugh Gurling verfasserin aut Andrew McQuillin verfasserin aut Rhian Gwilliam verfasserin aut Panos Deloukas verfasserin aut Ammar Al-Chalabi verfasserin aut Christopher E Shaw verfasserin aut Andrew B Singleton verfasserin aut Rita Guerreiro verfasserin aut Thomas W Mühleisen verfasserin aut Markus M Nöthen verfasserin aut Susanne Moebus verfasserin aut Karl-Heinz Jöckel verfasserin aut Norman Klopp verfasserin aut H-Erich Wichmann verfasserin aut Eckhard Rüther verfasserin aut Minerva M Carrasquillo verfasserin aut V Shane Pankratz verfasserin aut Steven G Younkin verfasserin aut John Hardy verfasserin aut Michael C O'Donovan verfasserin aut Michael J Owen verfasserin aut Julie Williams verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 5(2010), 11, p e13950 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:5 year:2010 number:11, p e13950 https://doi.org/10.1371/journal.pone.0013950 kostenfrei https://doaj.org/article/f60141a186cd4676b259fd600531e266 kostenfrei https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21085570/?tool=EBI kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2010 11, p e13950 |
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10.1371/journal.pone.0013950 doi (DE-627)DOAJ046502181 (DE-599)DOAJf60141a186cd4676b259fd600531e266 DE-627 ger DE-627 rakwb eng Lesley Jones verfasserin aut Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. Medicine R Science Q Peter A Holmans verfasserin aut Marian L Hamshere verfasserin aut Denise Harold verfasserin aut Valentina Moskvina verfasserin aut Dobril Ivanov verfasserin aut Andrew Pocklington verfasserin aut Richard Abraham verfasserin aut Paul Hollingworth verfasserin aut Rebecca Sims verfasserin aut Amy Gerrish verfasserin aut Jaspreet Singh Pahwa verfasserin aut Nicola Jones verfasserin aut Alexandra Stretton verfasserin aut Angharad R Morgan verfasserin aut Simon Lovestone verfasserin aut John Powell verfasserin aut Petroula Proitsi verfasserin aut Michelle K Lupton verfasserin aut Carol Brayne verfasserin aut David C Rubinsztein verfasserin aut Michael Gill verfasserin aut Brian Lawlor verfasserin aut Aoibhinn Lynch verfasserin aut Kevin Morgan verfasserin aut Kristelle S Brown verfasserin aut Peter A Passmore verfasserin aut David Craig verfasserin aut Bernadette McGuinness verfasserin aut Stephen Todd verfasserin aut Clive Holmes verfasserin aut David Mann verfasserin aut A David Smith verfasserin aut Seth Love verfasserin aut Patrick G Kehoe verfasserin aut Simon Mead verfasserin aut Nick Fox verfasserin aut Martin Rossor verfasserin aut John Collinge verfasserin aut Wolfgang Maier verfasserin aut Frank Jessen verfasserin aut Britta Schürmann verfasserin aut Reinhard Heun verfasserin aut Heike Kölsch verfasserin aut Hendrik van den Bussche verfasserin aut Isabella Heuser verfasserin aut Oliver Peters verfasserin aut Johannes Kornhuber verfasserin aut Jens Wiltfang verfasserin aut Martin Dichgans verfasserin aut Lutz Frölich verfasserin aut Harald Hampel verfasserin aut Michael Hüll verfasserin aut Dan Rujescu verfasserin aut Alison M Goate verfasserin aut John S K Kauwe verfasserin aut Carlos Cruchaga verfasserin aut Petra Nowotny verfasserin aut John C Morris verfasserin aut Kevin Mayo verfasserin aut Gill Livingston verfasserin aut Nicholas J Bass verfasserin aut Hugh Gurling verfasserin aut Andrew McQuillin verfasserin aut Rhian Gwilliam verfasserin aut Panos Deloukas verfasserin aut Ammar Al-Chalabi verfasserin aut Christopher E Shaw verfasserin aut Andrew B Singleton verfasserin aut Rita Guerreiro verfasserin aut Thomas W Mühleisen verfasserin aut Markus M Nöthen verfasserin aut Susanne Moebus verfasserin aut Karl-Heinz Jöckel verfasserin aut Norman Klopp verfasserin aut H-Erich Wichmann verfasserin aut Eckhard Rüther verfasserin aut Minerva M Carrasquillo verfasserin aut V Shane Pankratz verfasserin aut Steven G Younkin verfasserin aut John Hardy verfasserin aut Michael C O'Donovan verfasserin aut Michael J Owen verfasserin aut Julie Williams verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 5(2010), 11, p e13950 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:5 year:2010 number:11, p e13950 https://doi.org/10.1371/journal.pone.0013950 kostenfrei https://doaj.org/article/f60141a186cd4676b259fd600531e266 kostenfrei https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21085570/?tool=EBI kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2010 11, p e13950 |
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10.1371/journal.pone.0013950 doi (DE-627)DOAJ046502181 (DE-599)DOAJf60141a186cd4676b259fd600531e266 DE-627 ger DE-627 rakwb eng Lesley Jones verfasserin aut Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. Medicine R Science Q Peter A Holmans verfasserin aut Marian L Hamshere verfasserin aut Denise Harold verfasserin aut Valentina Moskvina verfasserin aut Dobril Ivanov verfasserin aut Andrew Pocklington verfasserin aut Richard Abraham verfasserin aut Paul Hollingworth verfasserin aut Rebecca Sims verfasserin aut Amy Gerrish verfasserin aut Jaspreet Singh Pahwa verfasserin aut Nicola Jones verfasserin aut Alexandra Stretton verfasserin aut Angharad R Morgan verfasserin aut Simon Lovestone verfasserin aut John Powell verfasserin aut Petroula Proitsi verfasserin aut Michelle K Lupton verfasserin aut Carol Brayne verfasserin aut David C Rubinsztein verfasserin aut Michael Gill verfasserin aut Brian Lawlor verfasserin aut Aoibhinn Lynch verfasserin aut Kevin Morgan verfasserin aut Kristelle S Brown verfasserin aut Peter A Passmore verfasserin aut David Craig verfasserin aut Bernadette McGuinness verfasserin aut Stephen Todd verfasserin aut Clive Holmes verfasserin aut David Mann verfasserin aut A David Smith verfasserin aut Seth Love verfasserin aut Patrick G Kehoe verfasserin aut Simon Mead verfasserin aut Nick Fox verfasserin aut Martin Rossor verfasserin aut John Collinge verfasserin aut Wolfgang Maier verfasserin aut Frank Jessen verfasserin aut Britta Schürmann verfasserin aut Reinhard Heun verfasserin aut Heike Kölsch verfasserin aut Hendrik van den Bussche verfasserin aut Isabella Heuser verfasserin aut Oliver Peters verfasserin aut Johannes Kornhuber verfasserin aut Jens Wiltfang verfasserin aut Martin Dichgans verfasserin aut Lutz Frölich verfasserin aut Harald Hampel verfasserin aut Michael Hüll verfasserin aut Dan Rujescu verfasserin aut Alison M Goate verfasserin aut John S K Kauwe verfasserin aut Carlos Cruchaga verfasserin aut Petra Nowotny verfasserin aut John C Morris verfasserin aut Kevin Mayo verfasserin aut Gill Livingston verfasserin aut Nicholas J Bass verfasserin aut Hugh Gurling verfasserin aut Andrew McQuillin verfasserin aut Rhian Gwilliam verfasserin aut Panos Deloukas verfasserin aut Ammar Al-Chalabi verfasserin aut Christopher E Shaw verfasserin aut Andrew B Singleton verfasserin aut Rita Guerreiro verfasserin aut Thomas W Mühleisen verfasserin aut Markus M Nöthen verfasserin aut Susanne Moebus verfasserin aut Karl-Heinz Jöckel verfasserin aut Norman Klopp verfasserin aut H-Erich Wichmann verfasserin aut Eckhard Rüther verfasserin aut Minerva M Carrasquillo verfasserin aut V Shane Pankratz verfasserin aut Steven G Younkin verfasserin aut John Hardy verfasserin aut Michael C O'Donovan verfasserin aut Michael J Owen verfasserin aut Julie Williams verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 5(2010), 11, p e13950 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:5 year:2010 number:11, p e13950 https://doi.org/10.1371/journal.pone.0013950 kostenfrei https://doaj.org/article/f60141a186cd4676b259fd600531e266 kostenfrei https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21085570/?tool=EBI kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2010 11, p e13950 |
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10.1371/journal.pone.0013950 doi (DE-627)DOAJ046502181 (DE-599)DOAJf60141a186cd4676b259fd600531e266 DE-627 ger DE-627 rakwb eng Lesley Jones verfasserin aut Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. Medicine R Science Q Peter A Holmans verfasserin aut Marian L Hamshere verfasserin aut Denise Harold verfasserin aut Valentina Moskvina verfasserin aut Dobril Ivanov verfasserin aut Andrew Pocklington verfasserin aut Richard Abraham verfasserin aut Paul Hollingworth verfasserin aut Rebecca Sims verfasserin aut Amy Gerrish verfasserin aut Jaspreet Singh Pahwa verfasserin aut Nicola Jones verfasserin aut Alexandra Stretton verfasserin aut Angharad R Morgan verfasserin aut Simon Lovestone verfasserin aut John Powell verfasserin aut Petroula Proitsi verfasserin aut Michelle K Lupton verfasserin aut Carol Brayne verfasserin aut David C Rubinsztein verfasserin aut Michael Gill verfasserin aut Brian Lawlor verfasserin aut Aoibhinn Lynch verfasserin aut Kevin Morgan verfasserin aut Kristelle S Brown verfasserin aut Peter A Passmore verfasserin aut David Craig verfasserin aut Bernadette McGuinness verfasserin aut Stephen Todd verfasserin aut Clive Holmes verfasserin aut David Mann verfasserin aut A David Smith verfasserin aut Seth Love verfasserin aut Patrick G Kehoe verfasserin aut Simon Mead verfasserin aut Nick Fox verfasserin aut Martin Rossor verfasserin aut John Collinge verfasserin aut Wolfgang Maier verfasserin aut Frank Jessen verfasserin aut Britta Schürmann verfasserin aut Reinhard Heun verfasserin aut Heike Kölsch verfasserin aut Hendrik van den Bussche verfasserin aut Isabella Heuser verfasserin aut Oliver Peters verfasserin aut Johannes Kornhuber verfasserin aut Jens Wiltfang verfasserin aut Martin Dichgans verfasserin aut Lutz Frölich verfasserin aut Harald Hampel verfasserin aut Michael Hüll verfasserin aut Dan Rujescu verfasserin aut Alison M Goate verfasserin aut John S K Kauwe verfasserin aut Carlos Cruchaga verfasserin aut Petra Nowotny verfasserin aut John C Morris verfasserin aut Kevin Mayo verfasserin aut Gill Livingston verfasserin aut Nicholas J Bass verfasserin aut Hugh Gurling verfasserin aut Andrew McQuillin verfasserin aut Rhian Gwilliam verfasserin aut Panos Deloukas verfasserin aut Ammar Al-Chalabi verfasserin aut Christopher E Shaw verfasserin aut Andrew B Singleton verfasserin aut Rita Guerreiro verfasserin aut Thomas W Mühleisen verfasserin aut Markus M Nöthen verfasserin aut Susanne Moebus verfasserin aut Karl-Heinz Jöckel verfasserin aut Norman Klopp verfasserin aut H-Erich Wichmann verfasserin aut Eckhard Rüther verfasserin aut Minerva M Carrasquillo verfasserin aut V Shane Pankratz verfasserin aut Steven G Younkin verfasserin aut John Hardy verfasserin aut Michael C O'Donovan verfasserin aut Michael J Owen verfasserin aut Julie Williams verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 5(2010), 11, p e13950 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:5 year:2010 number:11, p e13950 https://doi.org/10.1371/journal.pone.0013950 kostenfrei https://doaj.org/article/f60141a186cd4676b259fd600531e266 kostenfrei https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21085570/?tool=EBI kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2010 11, p e13950 |
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10.1371/journal.pone.0013950 doi (DE-627)DOAJ046502181 (DE-599)DOAJf60141a186cd4676b259fd600531e266 DE-627 ger DE-627 rakwb eng Lesley Jones verfasserin aut Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. Medicine R Science Q Peter A Holmans verfasserin aut Marian L Hamshere verfasserin aut Denise Harold verfasserin aut Valentina Moskvina verfasserin aut Dobril Ivanov verfasserin aut Andrew Pocklington verfasserin aut Richard Abraham verfasserin aut Paul Hollingworth verfasserin aut Rebecca Sims verfasserin aut Amy Gerrish verfasserin aut Jaspreet Singh Pahwa verfasserin aut Nicola Jones verfasserin aut Alexandra Stretton verfasserin aut Angharad R Morgan verfasserin aut Simon Lovestone verfasserin aut John Powell verfasserin aut Petroula Proitsi verfasserin aut Michelle K Lupton verfasserin aut Carol Brayne verfasserin aut David C Rubinsztein verfasserin aut Michael Gill verfasserin aut Brian Lawlor verfasserin aut Aoibhinn Lynch verfasserin aut Kevin Morgan verfasserin aut Kristelle S Brown verfasserin aut Peter A Passmore verfasserin aut David Craig verfasserin aut Bernadette McGuinness verfasserin aut Stephen Todd verfasserin aut Clive Holmes verfasserin aut David Mann verfasserin aut A David Smith verfasserin aut Seth Love verfasserin aut Patrick G Kehoe verfasserin aut Simon Mead verfasserin aut Nick Fox verfasserin aut Martin Rossor verfasserin aut John Collinge verfasserin aut Wolfgang Maier verfasserin aut Frank Jessen verfasserin aut Britta Schürmann verfasserin aut Reinhard Heun verfasserin aut Heike Kölsch verfasserin aut Hendrik van den Bussche verfasserin aut Isabella Heuser verfasserin aut Oliver Peters verfasserin aut Johannes Kornhuber verfasserin aut Jens Wiltfang verfasserin aut Martin Dichgans verfasserin aut Lutz Frölich verfasserin aut Harald Hampel verfasserin aut Michael Hüll verfasserin aut Dan Rujescu verfasserin aut Alison M Goate verfasserin aut John S K Kauwe verfasserin aut Carlos Cruchaga verfasserin aut Petra Nowotny verfasserin aut John C Morris verfasserin aut Kevin Mayo verfasserin aut Gill Livingston verfasserin aut Nicholas J Bass verfasserin aut Hugh Gurling verfasserin aut Andrew McQuillin verfasserin aut Rhian Gwilliam verfasserin aut Panos Deloukas verfasserin aut Ammar Al-Chalabi verfasserin aut Christopher E Shaw verfasserin aut Andrew B Singleton verfasserin aut Rita Guerreiro verfasserin aut Thomas W Mühleisen verfasserin aut Markus M Nöthen verfasserin aut Susanne Moebus verfasserin aut Karl-Heinz Jöckel verfasserin aut Norman Klopp verfasserin aut H-Erich Wichmann verfasserin aut Eckhard Rüther verfasserin aut Minerva M Carrasquillo verfasserin aut V Shane Pankratz verfasserin aut Steven G Younkin verfasserin aut John Hardy verfasserin aut Michael C O'Donovan verfasserin aut Michael J Owen verfasserin aut Julie Williams verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 5(2010), 11, p e13950 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:5 year:2010 number:11, p e13950 https://doi.org/10.1371/journal.pone.0013950 kostenfrei https://doaj.org/article/f60141a186cd4676b259fd600531e266 kostenfrei https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21085570/?tool=EBI kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2010 11, p e13950 |
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PLoS ONE |
authorswithroles_txt_mv |
Lesley Jones @@aut@@ Peter A Holmans @@aut@@ Marian L Hamshere @@aut@@ Denise Harold @@aut@@ Valentina Moskvina @@aut@@ Dobril Ivanov @@aut@@ Andrew Pocklington @@aut@@ Richard Abraham @@aut@@ Paul Hollingworth @@aut@@ Rebecca Sims @@aut@@ Amy Gerrish @@aut@@ Jaspreet Singh Pahwa @@aut@@ Nicola Jones @@aut@@ Alexandra Stretton @@aut@@ Angharad R Morgan @@aut@@ Simon Lovestone @@aut@@ John Powell @@aut@@ Petroula Proitsi @@aut@@ Michelle K Lupton @@aut@@ Carol Brayne @@aut@@ David C Rubinsztein @@aut@@ Michael Gill @@aut@@ Brian Lawlor @@aut@@ Aoibhinn Lynch @@aut@@ Kevin Morgan @@aut@@ Kristelle S Brown @@aut@@ Peter A Passmore @@aut@@ David Craig @@aut@@ Bernadette McGuinness @@aut@@ Stephen Todd @@aut@@ Clive Holmes @@aut@@ David Mann @@aut@@ A David Smith @@aut@@ Seth Love @@aut@@ Patrick G Kehoe @@aut@@ Simon Mead @@aut@@ Nick Fox @@aut@@ Martin Rossor @@aut@@ John Collinge @@aut@@ Wolfgang Maier @@aut@@ Frank Jessen @@aut@@ Britta Schürmann @@aut@@ Reinhard Heun @@aut@@ Heike Kölsch @@aut@@ Hendrik van den Bussche @@aut@@ Isabella Heuser @@aut@@ Oliver Peters @@aut@@ Johannes Kornhuber @@aut@@ Jens Wiltfang @@aut@@ Martin Dichgans @@aut@@ Lutz Frölich @@aut@@ Harald Hampel @@aut@@ Michael Hüll @@aut@@ Dan Rujescu @@aut@@ Alison M Goate @@aut@@ John S K Kauwe @@aut@@ Carlos Cruchaga @@aut@@ Petra Nowotny @@aut@@ John C Morris @@aut@@ Kevin Mayo @@aut@@ Gill Livingston @@aut@@ Nicholas J Bass @@aut@@ Hugh Gurling @@aut@@ Andrew McQuillin @@aut@@ Rhian Gwilliam @@aut@@ Panos Deloukas @@aut@@ Ammar Al-Chalabi @@aut@@ Christopher E Shaw @@aut@@ Andrew B Singleton @@aut@@ Rita Guerreiro @@aut@@ Thomas W Mühleisen @@aut@@ Markus M Nöthen @@aut@@ Susanne Moebus @@aut@@ Karl-Heinz Jöckel @@aut@@ Norman Klopp @@aut@@ H-Erich Wichmann @@aut@@ Eckhard Rüther @@aut@@ Minerva M Carrasquillo @@aut@@ V Shane Pankratz @@aut@@ Steven G Younkin @@aut@@ John Hardy @@aut@@ Michael C O'Donovan @@aut@@ Michael J Owen @@aut@@ Julie Williams @@aut@@ |
publishDateDaySort_date |
2010-01-01T00:00:00Z |
hierarchy_top_id |
523574592 |
id |
DOAJ046502181 |
language_de |
englisch |
fullrecord |
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Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. 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Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease |
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genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of alzheimer's disease |
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Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. |
abstract |
<h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. |
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<h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. |
abstract_unstemmed |
<h4<Background</h4<Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes.<h4<Methodology</h4<We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset.<h4<Principal findings</h4<We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD.<h4<Significance</h4<Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches. |
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Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. |
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|
score |
7.400591 |