Increased Menopausal Age Reduces the Risk of Parkinson's Disease: A Mendelian Randomization Approach
ABSTRACT Background Studies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian randomization (MR) may address measurement errors because of difficulties accurately reporting the age these life events occur. Objective...
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| Published in | Movement disorders Vol. 36; no. 10; pp. 2264 - 2272 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken, USA
John Wiley & Sons, Inc
01.10.2021
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | ABSTRACT
Background
Studies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian randomization (MR) may address measurement errors because of difficulties accurately reporting the age these life events occur.
Objective
We used MR to assess the association between age at menopause and age at menarche with PD risk.
Methods
We performed inverse variant‐weighted (IVW) MR analysis using external genome‐wide association study (GWAS) summary data from the United Kingdom biobank, and the effect estimates between genetic variants and PD among two population‐based studies (Parkinson's disease in Denmark (PASIDA) study, Denmark, and Parkinson's Environment and Gene study [PEG], United States) that enrolled 1737 female and 2430 male subjects of European ancestry. We, then, replicated our findings for age at menopause using summary statistics from the PD consortium (19 773 women), followed by a meta‐analysis combining all summary statistics.
Results
For each year increase in age at menopause, the risk for PD decreased (odds ration [OR], 0.84; 95% confidence interval [CI], 0.73–0.98; P = 0.03) among women in our study, whereas there was no association among men (OR, 0.98; 95% CI, 0.85–1.11; P = 0.71). A replication using summary statistics from the PD consortium estimated an OR of 0.94 (95% CI, 0.90–0.99; P = 0.01), and we calculated a meta‐analytic OR of 0.93 (95% CI, 0.89–0.98; P = 0.003). There was no indication for an association between age at menarche and PD (OR, 0.75; 95% CI, 0.44–1.29; P = 0.29).
Conclusions
A later age at menopause was associated with a decreased risk of PD in women, supporting the hypothesis that sex hormones or other factors related to late menopause may be neuroprotective in PD. © 2021 International Parkinson and Movement Disorder Society |
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| AbstractList | BackgroundStudies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian randomization (MR) may address measurement errors because of difficulties accurately reporting the age these life events occur.ObjectiveWe used MR to assess the association between age at menopause and age at menarche with PD risk.MethodsWe performed inverse variant‐weighted (IVW) MR analysis using external genome‐wide association study (GWAS) summary data from the United Kingdom biobank, and the effect estimates between genetic variants and PD among two population‐based studies (Parkinson's disease in Denmark (PASIDA) study, Denmark, and Parkinson's Environment and Gene study [PEG], United States) that enrolled 1737 female and 2430 male subjects of European ancestry. We, then, replicated our findings for age at menopause using summary statistics from the PD consortium (19 773 women), followed by a meta‐analysis combining all summary statistics.ResultsFor each year increase in age at menopause, the risk for PD decreased (odds ration [OR], 0.84; 95% confidence interval [CI], 0.73–0.98; P = 0.03) among women in our study, whereas there was no association among men (OR, 0.98; 95% CI, 0.85–1.11; P = 0.71). A replication using summary statistics from the PD consortium estimated an OR of 0.94 (95% CI, 0.90–0.99; P = 0.01), and we calculated a meta‐analytic OR of 0.93 (95% CI, 0.89–0.98; P = 0.003). There was no indication for an association between age at menarche and PD (OR, 0.75; 95% CI, 0.44–1.29; P = 0.29).ConclusionsA later age at menopause was associated with a decreased risk of PD in women, supporting the hypothesis that sex hormones or other factors related to late menopause may be neuroprotective in PD. © 2021 International Parkinson and Movement Disorder Society Studies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian randomization (MR) may address measurement errors because of difficulties accurately reporting the age these life events occur. We used MR to assess the association between age at menopause and age at menarche with PD risk. We performed inverse variant-weighted (IVW) MR analysis using external genome-wide association study (GWAS) summary data from the United Kingdom biobank, and the effect estimates between genetic variants and PD among two population-based studies (Parkinson's disease in Denmark (PASIDA) study, Denmark, and Parkinson's Environment and Gene study [PEG], United States) that enrolled 1737 female and 2430 male subjects of European ancestry. We, then, replicated our findings for age at menopause using summary statistics from the PD consortium (19 773 women), followed by a meta-analysis combining all summary statistics. For each year increase in age at menopause, the risk for PD decreased (odds ration [OR], 0.84; 95% confidence interval [CI], 0.73-0.98; P = 0.03) among women in our study, whereas there was no association among men (OR, 0.98; 95% CI, 0.85-1.11; P = 0.71). A replication using summary statistics from the PD consortium estimated an OR of 0.94 (95% CI, 0.90-0.99; P = 0.01), and we calculated a meta-analytic OR of 0.93 (95% CI, 0.89-0.98; P = 0.003). There was no indication for an association between age at menarche and PD (OR, 0.75; 95% CI, 0.44-1.29; P = 0.29). A later age at menopause was associated with a decreased risk of PD in women, supporting the hypothesis that sex hormones or other factors related to late menopause may be neuroprotective in PD. © 2021 International Parkinson and Movement Disorder Society. ABSTRACT Background Studies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian randomization (MR) may address measurement errors because of difficulties accurately reporting the age these life events occur. Objective We used MR to assess the association between age at menopause and age at menarche with PD risk. Methods We performed inverse variant‐weighted (IVW) MR analysis using external genome‐wide association study (GWAS) summary data from the United Kingdom biobank, and the effect estimates between genetic variants and PD among two population‐based studies (Parkinson's disease in Denmark (PASIDA) study, Denmark, and Parkinson's Environment and Gene study [PEG], United States) that enrolled 1737 female and 2430 male subjects of European ancestry. We, then, replicated our findings for age at menopause using summary statistics from the PD consortium (19 773 women), followed by a meta‐analysis combining all summary statistics. Results For each year increase in age at menopause, the risk for PD decreased (odds ration [OR], 0.84; 95% confidence interval [CI], 0.73–0.98; P = 0.03) among women in our study, whereas there was no association among men (OR, 0.98; 95% CI, 0.85–1.11; P = 0.71). A replication using summary statistics from the PD consortium estimated an OR of 0.94 (95% CI, 0.90–0.99; P = 0.01), and we calculated a meta‐analytic OR of 0.93 (95% CI, 0.89–0.98; P = 0.003). There was no indication for an association between age at menarche and PD (OR, 0.75; 95% CI, 0.44–1.29; P = 0.29). Conclusions A later age at menopause was associated with a decreased risk of PD in women, supporting the hypothesis that sex hormones or other factors related to late menopause may be neuroprotective in PD. © 2021 International Parkinson and Movement Disorder Society Studies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian randomization (MR) may address measurement errors because of difficulties accurately reporting the age these life events occur.BACKGROUNDStudies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian randomization (MR) may address measurement errors because of difficulties accurately reporting the age these life events occur.We used MR to assess the association between age at menopause and age at menarche with PD risk.OBJECTIVEWe used MR to assess the association between age at menopause and age at menarche with PD risk.We performed inverse variant-weighted (IVW) MR analysis using external genome-wide association study (GWAS) summary data from the United Kingdom biobank, and the effect estimates between genetic variants and PD among two population-based studies (Parkinson's disease in Denmark (PASIDA) study, Denmark, and Parkinson's Environment and Gene study [PEG], United States) that enrolled 1737 female and 2430 male subjects of European ancestry. We, then, replicated our findings for age at menopause using summary statistics from the PD consortium (19 773 women), followed by a meta-analysis combining all summary statistics.METHODSWe performed inverse variant-weighted (IVW) MR analysis using external genome-wide association study (GWAS) summary data from the United Kingdom biobank, and the effect estimates between genetic variants and PD among two population-based studies (Parkinson's disease in Denmark (PASIDA) study, Denmark, and Parkinson's Environment and Gene study [PEG], United States) that enrolled 1737 female and 2430 male subjects of European ancestry. We, then, replicated our findings for age at menopause using summary statistics from the PD consortium (19 773 women), followed by a meta-analysis combining all summary statistics.For each year increase in age at menopause, the risk for PD decreased (odds ration [OR], 0.84; 95% confidence interval [CI], 0.73-0.98; P = 0.03) among women in our study, whereas there was no association among men (OR, 0.98; 95% CI, 0.85-1.11; P = 0.71). A replication using summary statistics from the PD consortium estimated an OR of 0.94 (95% CI, 0.90-0.99; P = 0.01), and we calculated a meta-analytic OR of 0.93 (95% CI, 0.89-0.98; P = 0.003). There was no indication for an association between age at menarche and PD (OR, 0.75; 95% CI, 0.44-1.29; P = 0.29).RESULTSFor each year increase in age at menopause, the risk for PD decreased (odds ration [OR], 0.84; 95% confidence interval [CI], 0.73-0.98; P = 0.03) among women in our study, whereas there was no association among men (OR, 0.98; 95% CI, 0.85-1.11; P = 0.71). A replication using summary statistics from the PD consortium estimated an OR of 0.94 (95% CI, 0.90-0.99; P = 0.01), and we calculated a meta-analytic OR of 0.93 (95% CI, 0.89-0.98; P = 0.003). There was no indication for an association between age at menarche and PD (OR, 0.75; 95% CI, 0.44-1.29; P = 0.29).A later age at menopause was associated with a decreased risk of PD in women, supporting the hypothesis that sex hormones or other factors related to late menopause may be neuroprotective in PD. © 2021 International Parkinson and Movement Disorder Society.CONCLUSIONSA later age at menopause was associated with a decreased risk of PD in women, supporting the hypothesis that sex hormones or other factors related to late menopause may be neuroprotective in PD. © 2021 International Parkinson and Movement Disorder Society. |
| Author | Lill, Christina M. Kusters, Cynthia D.J. Keener, Adrienne M. Ritz, Beate R. Hansen, Johnni Sinsheimer, Janet S. Paul, Kimberly C. Bertram, Lars Horvath, Steve Duarte Folle, Aline Bronstein, Jeff M. |
| AuthorAffiliation | 9 Department of Biostatistics, School of Public Health, University of California, Los Angeles, Los Angeles, CA, USA 3 Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA, USA 7 Department of Psychology, Centre for Lifespan Changes in Brain and Cognition, University of Oslo, Oslo, Norway 1 Department of Human Genetics, David Geffen School of Medicine, Los Angeles, CA, USA 10 Department of Computational Medicine, David Geffen School of Medicine, Los Angeles, CA, USA 6 Lübeck Interdisciplinary Platform for Genome Analytics, University of Lübeck, Lübeck, Germany 8 Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark 12 Ageing Epidemiology Research Unit, School of Public Health, Imperial College, London, United Kingdom 4 Parkinson’s Disease Research, Education, and Clinical Center, Greater Los Angeles Veterans Affairs Medical Center, Los Angeles, California, USA 5 Brain Research Institute, University of California, Los Angeles, CA, USA 13 De |
| AuthorAffiliation_xml | – name: 12 Ageing Epidemiology Research Unit, School of Public Health, Imperial College, London, United Kingdom – name: 2 Department of Neurology, David Geffen School of Medicine, Los Angeles, CA, USA – name: 11 Translational Epidemiology Group, Lübeck Interdisciplinary Platform for Genome Analytics, University of Lübeck, Lübeck, Germany – name: 1 Department of Human Genetics, David Geffen School of Medicine, Los Angeles, CA, USA – name: 4 Parkinson’s Disease Research, Education, and Clinical Center, Greater Los Angeles Veterans Affairs Medical Center, Los Angeles, California, USA – name: 8 Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark – name: 9 Department of Biostatistics, School of Public Health, University of California, Los Angeles, Los Angeles, CA, USA – name: 5 Brain Research Institute, University of California, Los Angeles, CA, USA – name: 7 Department of Psychology, Centre for Lifespan Changes in Brain and Cognition, University of Oslo, Oslo, Norway – name: 10 Department of Computational Medicine, David Geffen School of Medicine, Los Angeles, CA, USA – name: 6 Lübeck Interdisciplinary Platform for Genome Analytics, University of Lübeck, Lübeck, Germany – name: 3 Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA, USA – name: 13 Department of Environmental Health, UCLA Fielding School of Public Health, Los Angeles, CA, USA |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34426982$$D View this record in MEDLINE/PubMed |
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| Copyright | 2021 International Parkinson and Movement Disorder Society 2021 International Parkinson and Movement Disorder Society. |
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| Keywords | Parkinson's disease Mendelian randomization menopause females menarche |
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| Notes | Funding sources Relevant conflicts of interest/financial disclosures C.M.L. and L.B. received funding from the German Research Foundation for the genome‐wide SNP data generation and processing of the PEG and PASIDA GWAS data (DFG; FOR2488/1: LI 2654/2‐1 and BE 2287/5‐1). C.M.L. received support by a “habilitation grant” (H01‐2019) from the University of Lübeck. J.S.S. was partially funded by NIH/NHGRI grant HG009120. This project has been made available with funding from National Institutes of Health (NIH) grants R01‐ES010544, R01‐ES013717, U54‐ES012078, P01‐ES016732, and P50‐NS038367; initial pilot funding from NIH P30‐ES07048; a Community Fast Track grant by the MJFox Foundation; a pilot grant by the American Parkinson Disease Association; and from the Parkinson's Alliance. C.K. is supported by the NIH grant F32AG063442. No conflicts of interest. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Beate R. Ritz was extensively involved in overseeing the project, gathering all required information (phenotypical and genetics data), the conception, organization and execution of the original PEG and PASIDA studies and this particular project, design and critiquing of the statistical analysis and in reviewing and critiquing the manuscript. Cynthia DJ Kusters: performed all parts of this project, including conception, organization, execution, statistical analysis and manuscript writing and editing Adrienne M Keener, Jeff M. Bronstein and Johnni Hansen were extensively involved in gathering of phenotypical data, reviewing and critiquing statistical analysis, and with the review and critiquing of the manuscript Authors’ Roles Lars Bertram and Christina M. Lill were critical in analyzing the genomic data for all patients, as well as reviewing and critiquing statistical and genetic analyses, and with the review and critiquing of the manuscript Kimberly C Paul and Aline Duarte Folle: have been extensively involved in the research project conception, organization and execution, design, review and critiquing of the statistical analysis, and review and critiques of the manuscript Steve Horvath, and Janet S. Sinsheimer were extensively involved in the design, execution and critiquing the statistical analysis, as well as review and critiquing of the manuscript. |
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Background
Studies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian... Studies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian randomization (MR) may... BackgroundStudies of Parkinson's disease (PD) and the association with age at menarche or menopause have reported inconsistent findings. Mendelian... |
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| SubjectTerms | Age Consortia Female females Genetic diversity Genome-wide association studies Genome-Wide Association Study Genomes Humans Male Menarche Mendelian randomization Mendelian Randomization Analysis Menopause Movement disorders Neurodegenerative diseases Neuroprotection Parkinson Disease - epidemiology Parkinson Disease - genetics Parkinson's disease Polymorphism, Single Nucleotide - genetics Population studies Population-based studies Risk Factors Sex hormones Statistical analysis Womens health |
| Title | Increased Menopausal Age Reduces the Risk of Parkinson's Disease: A Mendelian Randomization Approach |
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