Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study
Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no l...
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Übergeordnetes Werk: |
Enthalten in: The lancet |
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| Übergeordnetes Werk: |
volume:17 ; pages:64-74 |
| DOI / URN: |
10.1016/S1474-4422(17)30400-3 |
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| Katalog-ID: |
ELV000053031 |
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| 100 | 1 | |a Guerreiro, Rita |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study |
| 264 | 1 | |c 2018 | |
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| 520 | |a Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. | ||
| 700 | 1 | |a Ross, Owen A |e verfasserin |4 aut | |
| 700 | 1 | |a Kun-Rodrigues, Celia |e verfasserin |4 aut | |
| 700 | 1 | |a Hernandez, Dena G |e verfasserin |4 aut | |
| 700 | 1 | |a Orme, Tatiana |e verfasserin |4 aut | |
| 700 | 1 | |a Eicher, John D |e verfasserin |4 aut | |
| 700 | 1 | |a Shepherd, Claire E |e verfasserin |4 aut | |
| 700 | 1 | |a Parkkinen, Laura |e verfasserin |4 aut | |
| 700 | 1 | |a Darwent, Lee |e verfasserin |4 aut | |
| 700 | 1 | |a Heckman, Michael G |e verfasserin |4 aut | |
| 700 | 1 | |a Scholz, Sonja W |e verfasserin |4 aut | |
| 700 | 1 | |a Troncoso, Juan C |e verfasserin |4 aut | |
| 700 | 1 | |a Pletnikova, Olga |e verfasserin |4 aut | |
| 700 | 1 | |a Ansorge, Olaf |e verfasserin |4 aut | |
| 700 | 1 | |a Clarimon, Jordi |e verfasserin |4 aut | |
| 700 | 1 | |a Lleo, Alberto |e verfasserin |4 aut | |
| 700 | 1 | |a Morenas-Rodriguez, Estrella |e verfasserin |4 aut | |
| 700 | 1 | |a Clark, Lorraine |e verfasserin |4 aut | |
| 700 | 1 | |a Honig, Lawrence S |e verfasserin |4 aut | |
| 700 | 1 | |a Marder, Karen |e verfasserin |4 aut | |
| 700 | 1 | |a Lemstra, Afina |e verfasserin |4 aut | |
| 700 | 1 | |a Rogaeva, Ekaterina |e verfasserin |4 aut | |
| 700 | 1 | |a St George-Hyslop, Peter |e verfasserin |4 aut | |
| 700 | 1 | |a Londos, Elisabet |e verfasserin |4 aut | |
| 700 | 1 | |a Zetterberg, Henrik |e verfasserin |4 aut | |
| 700 | 1 | |a Barber, Imelda |e verfasserin |4 aut | |
| 700 | 1 | |a Braae, Anne |e verfasserin |4 aut | |
| 700 | 1 | |a Brown, Kristelle |e verfasserin |4 aut | |
| 700 | 1 | |a Morgan, Kevin |e verfasserin |4 aut | |
| 700 | 1 | |a Troakes, Claire |e verfasserin |4 aut | |
| 700 | 1 | |a Al-Sarraj, Safa |e verfasserin |4 aut | |
| 700 | 1 | |a Lashley, Tammaryn |e verfasserin |4 aut | |
| 700 | 1 | |a Holton, Janice |e verfasserin |4 aut | |
| 700 | 1 | |a Compta, Yaroslau |e verfasserin |4 aut | |
| 700 | 1 | |a Van Deerlin, Vivianna |e verfasserin |4 aut | |
| 700 | 1 | |a Serrano, Geidy E |e verfasserin |4 aut | |
| 700 | 1 | |a Beach, Thomas G |e verfasserin |4 aut | |
| 700 | 1 | |a Lesage, Suzanne |e verfasserin |4 aut | |
| 700 | 1 | |a Galasko, Douglas |e verfasserin |4 aut | |
| 700 | 1 | |a Masliah, Eliezer |e verfasserin |4 aut | |
| 700 | 1 | |a Santana, Isabel |e verfasserin |4 aut | |
| 700 | 1 | |a Pastor, Pau |e verfasserin |4 aut | |
| 700 | 1 | |a Diez-Fairen, Monica |e verfasserin |4 aut | |
| 700 | 1 | |a Aguilar, Miquel |e verfasserin |4 aut | |
| 700 | 1 | |a Tienari, Pentti J |e verfasserin |4 aut | |
| 700 | 1 | |a Myllykangas, Liisa |e verfasserin |4 aut | |
| 700 | 1 | |a Oinas, Minna |e verfasserin |4 aut | |
| 700 | 1 | |a Revesz, Tamas |e verfasserin |4 aut | |
| 700 | 1 | |a Lees, Andrew |e verfasserin |4 aut | |
| 700 | 1 | |a Boeve, Brad F |e verfasserin |4 aut | |
| 700 | 1 | |a Petersen, Ronald C |e verfasserin |4 aut | |
| 700 | 1 | |a Ferman, Tanis J |e verfasserin |4 aut | |
| 700 | 1 | |a Escott-Price, Valentina |e verfasserin |4 aut | |
| 700 | 1 | |a Graff-Radford, Neill |e verfasserin |4 aut | |
| 700 | 1 | |a Cairns, Nigel J |e verfasserin |4 aut | |
| 700 | 1 | |a Morris, John C |e verfasserin |4 aut | |
| 700 | 1 | |a Pickering-Brown, Stuart |e verfasserin |4 aut | |
| 700 | 1 | |a Mann, David |e verfasserin |4 aut | |
| 700 | 1 | |a Halliday, Glenda M |e verfasserin |4 aut | |
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| 700 | 1 | |a Trojanowski, John Q |e verfasserin |4 aut | |
| 700 | 1 | |a Dickson, Dennis W |e verfasserin |4 aut | |
| 700 | 1 | |a Singleton, Andrew |e verfasserin |4 aut | |
| 700 | 1 | |a Stone, David J |e verfasserin |4 aut | |
| 700 | 1 | |a Bras, Jose |e verfasserin |4 aut | |
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10.1016/S1474-4422(17)30400-3 doi (DE-627)ELV000053031 (ELSEVIER)S1474-4422(17)30400-3 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Guerreiro, Rita verfasserin aut Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. Ross, Owen A verfasserin aut Kun-Rodrigues, Celia verfasserin aut Hernandez, Dena G verfasserin aut Orme, Tatiana verfasserin aut Eicher, John D verfasserin aut Shepherd, Claire E verfasserin aut Parkkinen, Laura verfasserin aut Darwent, Lee verfasserin aut Heckman, Michael G verfasserin aut Scholz, Sonja W verfasserin aut Troncoso, Juan C verfasserin aut Pletnikova, Olga verfasserin aut Ansorge, Olaf verfasserin aut Clarimon, Jordi verfasserin aut Lleo, Alberto verfasserin aut Morenas-Rodriguez, Estrella verfasserin aut Clark, Lorraine verfasserin aut Honig, Lawrence S verfasserin aut Marder, Karen verfasserin aut Lemstra, Afina verfasserin aut Rogaeva, Ekaterina verfasserin aut St George-Hyslop, Peter verfasserin aut Londos, Elisabet verfasserin aut Zetterberg, Henrik verfasserin aut Barber, Imelda verfasserin aut Braae, Anne verfasserin aut Brown, Kristelle verfasserin aut Morgan, Kevin verfasserin aut Troakes, Claire verfasserin aut Al-Sarraj, Safa verfasserin aut Lashley, Tammaryn verfasserin aut Holton, Janice verfasserin aut Compta, Yaroslau verfasserin aut Van Deerlin, Vivianna verfasserin aut Serrano, Geidy E verfasserin aut Beach, Thomas G verfasserin aut Lesage, Suzanne verfasserin aut Galasko, Douglas verfasserin aut Masliah, Eliezer verfasserin aut Santana, Isabel verfasserin aut Pastor, Pau verfasserin aut Diez-Fairen, Monica verfasserin aut Aguilar, Miquel verfasserin aut Tienari, Pentti J verfasserin aut Myllykangas, Liisa verfasserin aut Oinas, Minna verfasserin aut Revesz, Tamas verfasserin aut Lees, Andrew verfasserin aut Boeve, Brad F verfasserin aut Petersen, Ronald C verfasserin aut Ferman, Tanis J verfasserin aut Escott-Price, Valentina verfasserin aut Graff-Radford, Neill verfasserin aut Cairns, Nigel J verfasserin aut Morris, John C verfasserin aut Pickering-Brown, Stuart verfasserin aut Mann, David verfasserin aut Halliday, Glenda M verfasserin aut Hardy, John verfasserin aut Trojanowski, John Q verfasserin aut Dickson, Dennis W verfasserin aut Singleton, Andrew verfasserin aut Stone, David J verfasserin aut Bras, Jose verfasserin aut Enthalten in The lancet <London> / Neurology London : Lancet Publ. Group, 2002 17, Seite 64-74 Online-Ressource (DE-627)348587104 (DE-600)2079704-7 (DE-576)110736362 1474-4465 nnns volume:17 pages:64-74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie AR 17 64-74 |
| spelling |
10.1016/S1474-4422(17)30400-3 doi (DE-627)ELV000053031 (ELSEVIER)S1474-4422(17)30400-3 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Guerreiro, Rita verfasserin aut Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. Ross, Owen A verfasserin aut Kun-Rodrigues, Celia verfasserin aut Hernandez, Dena G verfasserin aut Orme, Tatiana verfasserin aut Eicher, John D verfasserin aut Shepherd, Claire E verfasserin aut Parkkinen, Laura verfasserin aut Darwent, Lee verfasserin aut Heckman, Michael G verfasserin aut Scholz, Sonja W verfasserin aut Troncoso, Juan C verfasserin aut Pletnikova, Olga verfasserin aut Ansorge, Olaf verfasserin aut Clarimon, Jordi verfasserin aut Lleo, Alberto verfasserin aut Morenas-Rodriguez, Estrella verfasserin aut Clark, Lorraine verfasserin aut Honig, Lawrence S verfasserin aut Marder, Karen verfasserin aut Lemstra, Afina verfasserin aut Rogaeva, Ekaterina verfasserin aut St George-Hyslop, Peter verfasserin aut Londos, Elisabet verfasserin aut Zetterberg, Henrik verfasserin aut Barber, Imelda verfasserin aut Braae, Anne verfasserin aut Brown, Kristelle verfasserin aut Morgan, Kevin verfasserin aut Troakes, Claire verfasserin aut Al-Sarraj, Safa verfasserin aut Lashley, Tammaryn verfasserin aut Holton, Janice verfasserin aut Compta, Yaroslau verfasserin aut Van Deerlin, Vivianna verfasserin aut Serrano, Geidy E verfasserin aut Beach, Thomas G verfasserin aut Lesage, Suzanne verfasserin aut Galasko, Douglas verfasserin aut Masliah, Eliezer verfasserin aut Santana, Isabel verfasserin aut Pastor, Pau verfasserin aut Diez-Fairen, Monica verfasserin aut Aguilar, Miquel verfasserin aut Tienari, Pentti J verfasserin aut Myllykangas, Liisa verfasserin aut Oinas, Minna verfasserin aut Revesz, Tamas verfasserin aut Lees, Andrew verfasserin aut Boeve, Brad F verfasserin aut Petersen, Ronald C verfasserin aut Ferman, Tanis J verfasserin aut Escott-Price, Valentina verfasserin aut Graff-Radford, Neill verfasserin aut Cairns, Nigel J verfasserin aut Morris, John C verfasserin aut Pickering-Brown, Stuart verfasserin aut Mann, David verfasserin aut Halliday, Glenda M verfasserin aut Hardy, John verfasserin aut Trojanowski, John Q verfasserin aut Dickson, Dennis W verfasserin aut Singleton, Andrew verfasserin aut Stone, David J verfasserin aut Bras, Jose verfasserin aut Enthalten in The lancet <London> / Neurology London : Lancet Publ. Group, 2002 17, Seite 64-74 Online-Ressource (DE-627)348587104 (DE-600)2079704-7 (DE-576)110736362 1474-4465 nnns volume:17 pages:64-74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie AR 17 64-74 |
| allfields_unstemmed |
10.1016/S1474-4422(17)30400-3 doi (DE-627)ELV000053031 (ELSEVIER)S1474-4422(17)30400-3 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Guerreiro, Rita verfasserin aut Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. Ross, Owen A verfasserin aut Kun-Rodrigues, Celia verfasserin aut Hernandez, Dena G verfasserin aut Orme, Tatiana verfasserin aut Eicher, John D verfasserin aut Shepherd, Claire E verfasserin aut Parkkinen, Laura verfasserin aut Darwent, Lee verfasserin aut Heckman, Michael G verfasserin aut Scholz, Sonja W verfasserin aut Troncoso, Juan C verfasserin aut Pletnikova, Olga verfasserin aut Ansorge, Olaf verfasserin aut Clarimon, Jordi verfasserin aut Lleo, Alberto verfasserin aut Morenas-Rodriguez, Estrella verfasserin aut Clark, Lorraine verfasserin aut Honig, Lawrence S verfasserin aut Marder, Karen verfasserin aut Lemstra, Afina verfasserin aut Rogaeva, Ekaterina verfasserin aut St George-Hyslop, Peter verfasserin aut Londos, Elisabet verfasserin aut Zetterberg, Henrik verfasserin aut Barber, Imelda verfasserin aut Braae, Anne verfasserin aut Brown, Kristelle verfasserin aut Morgan, Kevin verfasserin aut Troakes, Claire verfasserin aut Al-Sarraj, Safa verfasserin aut Lashley, Tammaryn verfasserin aut Holton, Janice verfasserin aut Compta, Yaroslau verfasserin aut Van Deerlin, Vivianna verfasserin aut Serrano, Geidy E verfasserin aut Beach, Thomas G verfasserin aut Lesage, Suzanne verfasserin aut Galasko, Douglas verfasserin aut Masliah, Eliezer verfasserin aut Santana, Isabel verfasserin aut Pastor, Pau verfasserin aut Diez-Fairen, Monica verfasserin aut Aguilar, Miquel verfasserin aut Tienari, Pentti J verfasserin aut Myllykangas, Liisa verfasserin aut Oinas, Minna verfasserin aut Revesz, Tamas verfasserin aut Lees, Andrew verfasserin aut Boeve, Brad F verfasserin aut Petersen, Ronald C verfasserin aut Ferman, Tanis J verfasserin aut Escott-Price, Valentina verfasserin aut Graff-Radford, Neill verfasserin aut Cairns, Nigel J verfasserin aut Morris, John C verfasserin aut Pickering-Brown, Stuart verfasserin aut Mann, David verfasserin aut Halliday, Glenda M verfasserin aut Hardy, John verfasserin aut Trojanowski, John Q verfasserin aut Dickson, Dennis W verfasserin aut Singleton, Andrew verfasserin aut Stone, David J verfasserin aut Bras, Jose verfasserin aut Enthalten in The lancet <London> / Neurology London : Lancet Publ. Group, 2002 17, Seite 64-74 Online-Ressource (DE-627)348587104 (DE-600)2079704-7 (DE-576)110736362 1474-4465 nnns volume:17 pages:64-74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie AR 17 64-74 |
| allfieldsGer |
10.1016/S1474-4422(17)30400-3 doi (DE-627)ELV000053031 (ELSEVIER)S1474-4422(17)30400-3 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Guerreiro, Rita verfasserin aut Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. Ross, Owen A verfasserin aut Kun-Rodrigues, Celia verfasserin aut Hernandez, Dena G verfasserin aut Orme, Tatiana verfasserin aut Eicher, John D verfasserin aut Shepherd, Claire E verfasserin aut Parkkinen, Laura verfasserin aut Darwent, Lee verfasserin aut Heckman, Michael G verfasserin aut Scholz, Sonja W verfasserin aut Troncoso, Juan C verfasserin aut Pletnikova, Olga verfasserin aut Ansorge, Olaf verfasserin aut Clarimon, Jordi verfasserin aut Lleo, Alberto verfasserin aut Morenas-Rodriguez, Estrella verfasserin aut Clark, Lorraine verfasserin aut Honig, Lawrence S verfasserin aut Marder, Karen verfasserin aut Lemstra, Afina verfasserin aut Rogaeva, Ekaterina verfasserin aut St George-Hyslop, Peter verfasserin aut Londos, Elisabet verfasserin aut Zetterberg, Henrik verfasserin aut Barber, Imelda verfasserin aut Braae, Anne verfasserin aut Brown, Kristelle verfasserin aut Morgan, Kevin verfasserin aut Troakes, Claire verfasserin aut Al-Sarraj, Safa verfasserin aut Lashley, Tammaryn verfasserin aut Holton, Janice verfasserin aut Compta, Yaroslau verfasserin aut Van Deerlin, Vivianna verfasserin aut Serrano, Geidy E verfasserin aut Beach, Thomas G verfasserin aut Lesage, Suzanne verfasserin aut Galasko, Douglas verfasserin aut Masliah, Eliezer verfasserin aut Santana, Isabel verfasserin aut Pastor, Pau verfasserin aut Diez-Fairen, Monica verfasserin aut Aguilar, Miquel verfasserin aut Tienari, Pentti J verfasserin aut Myllykangas, Liisa verfasserin aut Oinas, Minna verfasserin aut Revesz, Tamas verfasserin aut Lees, Andrew verfasserin aut Boeve, Brad F verfasserin aut Petersen, Ronald C verfasserin aut Ferman, Tanis J verfasserin aut Escott-Price, Valentina verfasserin aut Graff-Radford, Neill verfasserin aut Cairns, Nigel J verfasserin aut Morris, John C verfasserin aut Pickering-Brown, Stuart verfasserin aut Mann, David verfasserin aut Halliday, Glenda M verfasserin aut Hardy, John verfasserin aut Trojanowski, John Q verfasserin aut Dickson, Dennis W verfasserin aut Singleton, Andrew verfasserin aut Stone, David J verfasserin aut Bras, Jose verfasserin aut Enthalten in The lancet <London> / Neurology London : Lancet Publ. Group, 2002 17, Seite 64-74 Online-Ressource (DE-627)348587104 (DE-600)2079704-7 (DE-576)110736362 1474-4465 nnns volume:17 pages:64-74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie AR 17 64-74 |
| allfieldsSound |
10.1016/S1474-4422(17)30400-3 doi (DE-627)ELV000053031 (ELSEVIER)S1474-4422(17)30400-3 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Guerreiro, Rita verfasserin aut Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. Ross, Owen A verfasserin aut Kun-Rodrigues, Celia verfasserin aut Hernandez, Dena G verfasserin aut Orme, Tatiana verfasserin aut Eicher, John D verfasserin aut Shepherd, Claire E verfasserin aut Parkkinen, Laura verfasserin aut Darwent, Lee verfasserin aut Heckman, Michael G verfasserin aut Scholz, Sonja W verfasserin aut Troncoso, Juan C verfasserin aut Pletnikova, Olga verfasserin aut Ansorge, Olaf verfasserin aut Clarimon, Jordi verfasserin aut Lleo, Alberto verfasserin aut Morenas-Rodriguez, Estrella verfasserin aut Clark, Lorraine verfasserin aut Honig, Lawrence S verfasserin aut Marder, Karen verfasserin aut Lemstra, Afina verfasserin aut Rogaeva, Ekaterina verfasserin aut St George-Hyslop, Peter verfasserin aut Londos, Elisabet verfasserin aut Zetterberg, Henrik verfasserin aut Barber, Imelda verfasserin aut Braae, Anne verfasserin aut Brown, Kristelle verfasserin aut Morgan, Kevin verfasserin aut Troakes, Claire verfasserin aut Al-Sarraj, Safa verfasserin aut Lashley, Tammaryn verfasserin aut Holton, Janice verfasserin aut Compta, Yaroslau verfasserin aut Van Deerlin, Vivianna verfasserin aut Serrano, Geidy E verfasserin aut Beach, Thomas G verfasserin aut Lesage, Suzanne verfasserin aut Galasko, Douglas verfasserin aut Masliah, Eliezer verfasserin aut Santana, Isabel verfasserin aut Pastor, Pau verfasserin aut Diez-Fairen, Monica verfasserin aut Aguilar, Miquel verfasserin aut Tienari, Pentti J verfasserin aut Myllykangas, Liisa verfasserin aut Oinas, Minna verfasserin aut Revesz, Tamas verfasserin aut Lees, Andrew verfasserin aut Boeve, Brad F verfasserin aut Petersen, Ronald C verfasserin aut Ferman, Tanis J verfasserin aut Escott-Price, Valentina verfasserin aut Graff-Radford, Neill verfasserin aut Cairns, Nigel J verfasserin aut Morris, John C verfasserin aut Pickering-Brown, Stuart verfasserin aut Mann, David verfasserin aut Halliday, Glenda M verfasserin aut Hardy, John verfasserin aut Trojanowski, John Q verfasserin aut Dickson, Dennis W verfasserin aut Singleton, Andrew verfasserin aut Stone, David J verfasserin aut Bras, Jose verfasserin aut Enthalten in The lancet <London> / Neurology London : Lancet Publ. Group, 2002 17, Seite 64-74 Online-Ressource (DE-627)348587104 (DE-600)2079704-7 (DE-576)110736362 1474-4465 nnns volume:17 pages:64-74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie AR 17 64-74 |
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Guerreiro, Rita @@aut@@ Ross, Owen A @@aut@@ Kun-Rodrigues, Celia @@aut@@ Hernandez, Dena G @@aut@@ Orme, Tatiana @@aut@@ Eicher, John D @@aut@@ Shepherd, Claire E @@aut@@ Parkkinen, Laura @@aut@@ Darwent, Lee @@aut@@ Heckman, Michael G @@aut@@ Scholz, Sonja W @@aut@@ Troncoso, Juan C @@aut@@ Pletnikova, Olga @@aut@@ Ansorge, Olaf @@aut@@ Clarimon, Jordi @@aut@@ Lleo, Alberto @@aut@@ Morenas-Rodriguez, Estrella @@aut@@ Clark, Lorraine @@aut@@ Honig, Lawrence S @@aut@@ Marder, Karen @@aut@@ Lemstra, Afina @@aut@@ Rogaeva, Ekaterina @@aut@@ St George-Hyslop, Peter @@aut@@ Londos, Elisabet @@aut@@ Zetterberg, Henrik @@aut@@ Barber, Imelda @@aut@@ Braae, Anne @@aut@@ Brown, Kristelle @@aut@@ Morgan, Kevin @@aut@@ Troakes, Claire @@aut@@ Al-Sarraj, Safa @@aut@@ Lashley, Tammaryn @@aut@@ Holton, Janice @@aut@@ Compta, Yaroslau @@aut@@ Van Deerlin, Vivianna @@aut@@ Serrano, Geidy E @@aut@@ Beach, Thomas G @@aut@@ Lesage, Suzanne @@aut@@ Galasko, Douglas @@aut@@ Masliah, Eliezer @@aut@@ Santana, Isabel @@aut@@ Pastor, Pau @@aut@@ Diez-Fairen, Monica @@aut@@ Aguilar, Miquel @@aut@@ Tienari, Pentti J @@aut@@ Myllykangas, Liisa @@aut@@ Oinas, Minna @@aut@@ Revesz, Tamas @@aut@@ Lees, Andrew @@aut@@ Boeve, Brad F @@aut@@ Petersen, Ronald C @@aut@@ Ferman, Tanis J @@aut@@ Escott-Price, Valentina @@aut@@ Graff-Radford, Neill @@aut@@ Cairns, Nigel J @@aut@@ Morris, John C @@aut@@ Pickering-Brown, Stuart @@aut@@ Mann, David @@aut@@ Halliday, Glenda M @@aut@@ Hardy, John @@aut@@ Trojanowski, John Q @@aut@@ Dickson, Dennis W @@aut@@ Singleton, Andrew @@aut@@ Stone, David J @@aut@@ Bras, Jose @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV000053031</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230524141418.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230427s2018 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/S1474-4422(17)30400-3</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV000053031</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1474-4422(17)30400-3</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rda</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Guerreiro, Rita</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ross, Owen A</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kun-Rodrigues, Celia</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hernandez, Dena G</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Orme, Tatiana</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Eicher, John D</subfield><subfield code="e">verfasserin</subfield><subfield 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Guerreiro, Rita |
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Guerreiro, Rita ddc 610 bkl 44.90 Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study |
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610 DE-600 44.90 bkl Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study |
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Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study |
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Guerreiro, Rita Ross, Owen A Kun-Rodrigues, Celia Hernandez, Dena G Orme, Tatiana Eicher, John D Shepherd, Claire E Parkkinen, Laura Darwent, Lee Heckman, Michael G Scholz, Sonja W Troncoso, Juan C Pletnikova, Olga Ansorge, Olaf Clarimon, Jordi Lleo, Alberto Morenas-Rodriguez, Estrella Clark, Lorraine Honig, Lawrence S Marder, Karen Lemstra, Afina Rogaeva, Ekaterina St George-Hyslop, Peter Londos, Elisabet Zetterberg, Henrik Barber, Imelda Braae, Anne Brown, Kristelle Morgan, Kevin Troakes, Claire Al-Sarraj, Safa Lashley, Tammaryn Holton, Janice Compta, Yaroslau Van Deerlin, Vivianna Serrano, Geidy E Beach, Thomas G Lesage, Suzanne Galasko, Douglas Masliah, Eliezer Santana, Isabel Pastor, Pau Diez-Fairen, Monica Aguilar, Miquel Tienari, Pentti J Myllykangas, Liisa Oinas, Minna Revesz, Tamas Lees, Andrew Boeve, Brad F Petersen, Ronald C Ferman, Tanis J Escott-Price, Valentina Graff-Radford, Neill Cairns, Nigel J Morris, John C Pickering-Brown, Stuart Mann, David Halliday, Glenda M Hardy, John Trojanowski, John Q Dickson, Dennis W Singleton, Andrew Stone, David J Bras, Jose |
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investigating the genetic architecture of dementia with lewy bodies: a two-stage genome-wide association study |
| title_auth |
Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study |
| abstract |
Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. |
| abstractGer |
Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. |
| abstract_unstemmed |
Background: Dementia with Lewy bodies is the second most common form of dementia in elderly people but has been overshadowed in the research field, partly because of similarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. So far, to our knowledge, no large-scale genetic study of dementia with Lewy bodies has been done. To better understand the genetic basis of dementia with Lewy bodies, we have done a genome-wide association study with the aim of identifying genetic risk factors for this disorder.Methods: In this two-stage genome-wide association study, we collected samples from white participants of European ancestry who had been diagnosed with dementia with Lewy bodies according to established clinical or pathological criteria. In the discovery stage (with the case cohort recruited from 22 centres in ten countries and the controls derived from two publicly available database of Genotypes and Phenotypes studies [phs000404.v1.p1 and phs000982.v1.p1] in the USA), we performed genotyping and exploited the recently established Haplotype Reference Consortium panel as the basis for imputation. Pathological samples were ascertained following autopsy in each individual brain bank, whereas clinical samples were collected after participant examination. There was no specific timeframe for collection of samples. We did association analyses in all participants with dementia with Lewy bodies, and also only in participants with pathological diagnosis. In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. Lastly, we did a meta-analysis of both stages under a fixed-effects model and used logistic regression to test for association in each stage.Findings: This study included 1743 patients with dementia with Lewy bodies (1324 with pathological diagnosis) and 4454 controls (1216 patients with dementia with Lewy bodies vs 3791 controls in the discovery stage; 527 vs 663 in the replication stage). Results confirm previously reported associations: APOE (rs429358; odds ratio [OR] 2·40, 95% CI 2·14–2·70; p=1·05 × 10−48), SNCA (rs7681440; OR 0·73, 0·66–0·81; p=6·39 × 10−10), an GBA (rs35749011; OR 2·55, 1·88–3·46; p=1·78 × 10−9). They also provide some evidence for a novel candidate locus, namely CNTN1 (rs7314908; OR 1·51, 1·27–1·79; p=2·32 × 10−6); further replication will be important. Additionally, we estimate the heritable component of dementia with Lewy bodies to be about 36%.Interpretation: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, we present the most comprehensive and well powered genetic study in dementia with Lewy bodies so far. These data show that common genetic variability has a role in the disease.Funding: The Alzheimer's Society and the Lewy Body Society. |
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Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study |
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Ross, Owen A Kun-Rodrigues, Celia Hernandez, Dena G Orme, Tatiana Eicher, John D Shepherd, Claire E Parkkinen, Laura Darwent, Lee Heckman, Michael G Scholz, Sonja W Troncoso, Juan C Pletnikova, Olga Ansorge, Olaf Clarimon, Jordi Lleo, Alberto Morenas-Rodriguez, Estrella Clark, Lorraine Honig, Lawrence S Marder, Karen Lemstra, Afina Rogaeva, Ekaterina St George-Hyslop, Peter Londos, Elisabet Zetterberg, Henrik Barber, Imelda Braae, Anne Brown, Kristelle Morgan, Kevin Troakes, Claire Al-Sarraj, Safa Lashley, Tammaryn Holton, Janice Compta, Yaroslau Van Deerlin, Vivianna Serrano, Geidy E Beach, Thomas G Lesage, Suzanne Galasko, Douglas Masliah, Eliezer Santana, Isabel Pastor, Pau Diez-Fairen, Monica Aguilar, Miquel Tienari, Pentti J Myllykangas, Liisa Oinas, Minna Revesz, Tamas Lees, Andrew Boeve, Brad F Petersen, Ronald C Ferman, Tanis J Escott-Price, Valentina Graff-Radford, Neill Cairns, Nigel J Morris, John C Pickering-Brown, Stuart Mann, David Halliday, Glenda M Hardy, John Trojanowski, John Q Dickson, Dennis W Singleton, Andrew Stone, David J Bras, Jose |
| author2Str |
Ross, Owen A Kun-Rodrigues, Celia Hernandez, Dena G Orme, Tatiana Eicher, John D Shepherd, Claire E Parkkinen, Laura Darwent, Lee Heckman, Michael G Scholz, Sonja W Troncoso, Juan C Pletnikova, Olga Ansorge, Olaf Clarimon, Jordi Lleo, Alberto Morenas-Rodriguez, Estrella Clark, Lorraine Honig, Lawrence S Marder, Karen Lemstra, Afina Rogaeva, Ekaterina St George-Hyslop, Peter Londos, Elisabet Zetterberg, Henrik Barber, Imelda Braae, Anne Brown, Kristelle Morgan, Kevin Troakes, Claire Al-Sarraj, Safa Lashley, Tammaryn Holton, Janice Compta, Yaroslau Van Deerlin, Vivianna Serrano, Geidy E Beach, Thomas G Lesage, Suzanne Galasko, Douglas Masliah, Eliezer Santana, Isabel Pastor, Pau Diez-Fairen, Monica Aguilar, Miquel Tienari, Pentti J Myllykangas, Liisa Oinas, Minna Revesz, Tamas Lees, Andrew Boeve, Brad F Petersen, Ronald C Ferman, Tanis J Escott-Price, Valentina Graff-Radford, Neill Cairns, Nigel J Morris, John C Pickering-Brown, Stuart Mann, David Halliday, Glenda M Hardy, John Trojanowski, John Q Dickson, Dennis W Singleton, Andrew Stone, David J Bras, Jose |
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| doi_str |
10.1016/S1474-4422(17)30400-3 |
| up_date |
2024-07-06T16:42:34.483Z |
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| score |
7.3985004 |