Abstract
The similarities between dementia with Lewy bodies (DLB) and both Parkinson's disease (PD) and Alzheimer's disease (AD) are many and range from clinical presentation, to neuropathological characteristics, to more recently identified, genetic determinants of risk. Because of these overlapping features, diagnosing DLB is challenging and has clinical implications since some therapeutic agents that are applicable in other diseases have adverse effects in DLB. Having shown that DLB shares some genetic risk with PD and AD, we have now quantified the amount of sharing through the application of genetic correlation estimates, and show that, from a purely genetic perspective, and excluding the strong association at the APOE locus, DLB is equally correlated to AD and PD.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 214.e7-214.e10 |
| Journal | Neurobiology of aging |
| Volume | 38 |
| DOIs | |
| State | Published - Oct 13 2016 |
Keywords
- Alzheimer's disease
- Dementia with Lewy bodies
- Genetic correlation
- Parkinson's disease
ASJC Scopus subject areas
- Neuroscience(all)
- Aging
- Clinical Neurology
- Developmental Biology
- Geriatrics and Gerontology
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Genome-wide analysis of genetic correlation in dementia with Lewy bodies, Parkinson's and Alzheimer's diseases. / International Parkinson's Disease Genomics Consortium (IPDGC).
In: Neurobiology of aging, Vol. 38, 13.10.2016, p. 214.e7-214.e10.Research output: Contribution to journal › Article › peer-review
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TY - JOUR
T1 - Genome-wide analysis of genetic correlation in dementia with Lewy bodies, Parkinson's and Alzheimer's diseases
AU - International Parkinson's Disease Genomics Consortium (IPDGC)
AU - Guerreiro, Rita
AU - Escott-Price, Valentina
AU - Darwent, Lee
AU - Parkkinen, Laura
AU - Ansorge, Olaf
AU - Hernandez, Dena G.
AU - Nalls, Michael A.
AU - Clark, Lorraine
AU - Honig, Lawrence
AU - Marder, Karen
AU - van der Flier, Wiesje
AU - Holstege, Henne
AU - Louwersheimer, Eva
AU - Lemstra, Afina
AU - Scheltens, Philip
AU - Rogaeva, Ekaterina
AU - St George-Hyslop, Peter
AU - Londos, Elisabet
AU - Zetterberg, Henrik
AU - Ortega-Cubero, Sara
AU - Pastor, Pau
AU - Ferman, Tanis J.
AU - Graff-Radford, Neill R.
AU - Ross, Owen A.
AU - Barber, Imelda
AU - Braae, Anne
AU - Brown, Kristelle
AU - Morgan, Kevin
AU - Maetzler, Walter
AU - Berg, Daniela
AU - Troakes, Claire
AU - Al-Sarraj, Safa
AU - Lashley, Tammaryn
AU - Compta, Yaroslau
AU - Revesz, Tamas
AU - Lees, Andrew
AU - Cairns, Nigel J.
AU - Halliday, Glenda M.
AU - Mann, David
AU - Pickering-Brown, Stuart
AU - Powell, John
AU - Lunnon, Katie
AU - Lupton, Michelle K.
AU - Dickson, Dennis
AU - Hardy, John
AU - Singleton, Andrew
AU - Bras, Jose
N1 - Funding Information: Rita Guerreiro and Jose Bras are supported by Research Fellowships from the Alzheimer's Society. This work was supported in part by a Parkinson's UK Innovation Award (K-1204) in collaboration with the Lewy Body Society and by the Wellcome Trust/MRC Joint Call in Neurodegeneration award (WT089698) to the UK Parkinson's Disease Consortium whose members are from the UCL Institute of Neurology, the University of Sheffield, and the MRC Protein Phosphorylation Unit at the University of Dundee and by an anonymous Foundation. The authors would like to acknowledge Elena Lorenzo for her technical assistance. This study was supported in part by grants from the Spanish Ministry of Science and Innovation SAF2006-10126 (2006–2009) and SAF2010-22329-C02-01 (2011–2013) and SAF2013-47939-R (2013–2015) to Pau Pastor and by the UTE project FIMA to Pau Pastor. They acknowledge the Oxford Brain Bank, supported by the Medical Research Council (MRC), Brains for Dementia Research (BDR) (Alzheimer Society and Alzheimer Research UK), Autistica UK, and the NIHR Oxford Biomedical Research Centre. The sample collection and database of the Amsterdam Dementia Cohort was funded by Stichting Dioraphte and Stichting VUMC fonds. Glenda M. Halliday is a Senior Principal Research Fellow of the National Health and Medical Research Council of Australia. For the neuropathologically confirmed samples from Australia, brain tissue was received from the Sydney Brain Bank, which is supported by Neuroscience Research Australia, the University of New South Wales, and the National Health and Medical Research Council of Australia. This study was also partially funded by the Wellcome Trust , Medical Research Council , Canadian Institutes of Health Research , Ontario Research Fund . The Nottingham Genetics Group is supported by ARUK and The Big Lottery Fund. The effort from Columbia University was supported by the Taub Institute , the Panasci Fund , the Parkinson's Disease Foundation , and NIH grants NS060113 (Lorraine Clark), P50AG008702 (P.I. Scott Small), P50NS038370 (P.I. R. Burke), and UL1TR000040 (P.I. H. Ginsberg). Owen A. Ross is supported by the Michael J. Fox Foundation, NINDS R01# NS078086. The Mayo Clinic Jacksonville is a Morris K. Udall Parkinson's Disease Research Center of Excellence (NINDS P50 #NS072187) and is supported by the Mangurian Foundation for Lewy body research. This work has received support from The Queen Square Brain Bank at the UCL Institute of Neurology. Some of the tissue samples studies were provided by the MRC London Neurodegenerative Diseases Brain Bank and the Brains for Dementia Research project (funded by Alzheimer's Society and ARUK). This research was supported in part by the NIHR UCLH Biomedical Research Centre , the Queen Square Dementia Biomedical Research Unit, the National Institute for Health Research (NIHR) Dementia Biomedical Research Unit and Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College Hospital , London. This work was supported in part by the Intramural Research Program of the National Institute on Aging, National Institutes of Health, Department of Health and Human Services; project AG000951-12. Funding to pay the Open Access publication charges for this article was provided by the Wellcome Trust and the Medical Research Council. Funding Information: Rita Guerreiro and Jose Bras are supported by Research Fellowships from the Alzheimer's Society. This work was supported in part by a Parkinson's UK Innovation Award (K-1204) in collaboration with the Lewy Body Society and by the Wellcome Trust/MRC Joint Call in Neurodegeneration award (WT089698) to the UK Parkinson's Disease Consortium whose members are from the UCL Institute of Neurology, the University of Sheffield, and the MRC Protein Phosphorylation Unit at the University of Dundee and by an anonymous Foundation. The authors would like to acknowledge Elena Lorenzo for her technical assistance. This study was supported in part by grants from the Spanish Ministry of Science and Innovation SAF2006-10126 (2006?2009) and SAF2010-22329-C02-01 (2011?2013) and SAF2013-47939-R (2013?2015) to Pau Pastor and by the UTE project FIMA to Pau Pastor. They acknowledge the Oxford Brain Bank, supported by the Medical Research Council (MRC), Brains for Dementia Research (BDR) (Alzheimer Society and Alzheimer Research UK), Autistica UK, and the NIHR Oxford Biomedical Research Centre. The sample collection and database of the Amsterdam Dementia Cohort was funded by Stichting Dioraphte and Stichting VUMC fonds. Glenda M. Halliday is a Senior Principal Research Fellow of the National Health and Medical Research Council of Australia. For the neuropathologically confirmed samples from Australia, brain tissue was received from the Sydney Brain Bank, which is supported by Neuroscience Research Australia, the University of New South Wales, and the National Health and Medical Research Council of Australia. This study was also partially funded by the Wellcome Trust, Medical Research Council, Canadian Institutes of Health Research, Ontario Research Fund. The Nottingham Genetics Group is supported by ARUK and The Big Lottery Fund. The effort from Columbia University was supported by the Taub Institute, the Panasci Fund, the Parkinson's Disease Foundation, and NIH grants NS060113 (Lorraine Clark), P50AG008702 (P.I. Scott Small), P50NS038370 (P.I. R. Burke), and UL1TR000040 (P.I. H. Ginsberg). Owen A. Ross is supported by the Michael J. Fox Foundation, NINDS R01# NS078086. The Mayo Clinic Jacksonville is a Morris K. Udall Parkinson's Disease Research Center of Excellence (NINDS P50 #NS072187) and is supported by the Mangurian Foundation for Lewy body research. This work has received support from The Queen Square Brain Bank at the UCL Institute of Neurology. Some of the tissue samples studies were provided by the MRC London Neurodegenerative Diseases Brain Bank and the Brains for Dementia Research project (funded by Alzheimer's Society and ARUK). This research was supported in part by the NIHR UCLH Biomedical Research Centre, the Queen Square Dementia Biomedical Research Unit, the National Institute for Health Research (NIHR) Dementia Biomedical Research Unit and Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College Hospital, London. This work was supported in part by the Intramural Research Program of the National Institute on Aging, National Institutes of Health, Department of Health and Human Services; project AG000951-12. Funding to pay the Open Access publication charges for this article was provided by the Wellcome Trust and the Medical Research Council. Publisher Copyright: © 2016 The Authors.
PY - 2016/10/13
Y1 - 2016/10/13
N2 - The similarities between dementia with Lewy bodies (DLB) and both Parkinson's disease (PD) and Alzheimer's disease (AD) are many and range from clinical presentation, to neuropathological characteristics, to more recently identified, genetic determinants of risk. Because of these overlapping features, diagnosing DLB is challenging and has clinical implications since some therapeutic agents that are applicable in other diseases have adverse effects in DLB. Having shown that DLB shares some genetic risk with PD and AD, we have now quantified the amount of sharing through the application of genetic correlation estimates, and show that, from a purely genetic perspective, and excluding the strong association at the APOE locus, DLB is equally correlated to AD and PD.
AB - The similarities between dementia with Lewy bodies (DLB) and both Parkinson's disease (PD) and Alzheimer's disease (AD) are many and range from clinical presentation, to neuropathological characteristics, to more recently identified, genetic determinants of risk. Because of these overlapping features, diagnosing DLB is challenging and has clinical implications since some therapeutic agents that are applicable in other diseases have adverse effects in DLB. Having shown that DLB shares some genetic risk with PD and AD, we have now quantified the amount of sharing through the application of genetic correlation estimates, and show that, from a purely genetic perspective, and excluding the strong association at the APOE locus, DLB is equally correlated to AD and PD.
KW - Alzheimer's disease
KW - Dementia with Lewy bodies
KW - Genetic correlation
KW - Parkinson's disease
UR - http://www.scopus.com/inward/record.url?scp=84948808791&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84948808791&partnerID=8YFLogxK
U2 - 10.1016/j.neurobiolaging.2015.10.028
DO - 10.1016/j.neurobiolaging.2015.10.028
M3 - Article
C2 - 26643944
AN - SCOPUS:84948808791
VL - 38
SP - 214.e7-214.e10
JO - Neurobiology of Aging
JF - Neurobiology of Aging
SN - 0197-4580
ER -