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6. A systematic analysis of the contribution of genetics to multimorbidity and comparisons with primary care data

Author

Murrin, Olivia, primary, Mounier, Ninon, additional, Voller, Bethany, additional, Tata, Linus, additional, Gallego-Moll, Carlos, additional, Roso-Llorach, Albert, additional, Carrasco-Ribelles, Lucía A, additional, Fox, Chris, additional, Allan, Louise M, additional, Woodward, Ruby M, additional, Liang, Xiaoran, additional, Valderas, Jose M, additional, Khalid, Sara, additional, Dudbridge, Frank, additional, Lamb, Sally E, additional, Mancini, Mary, additional, Farmer, Leon, additional, Boddy, Kate, additional, Bowden, Jack, additional, Melzer, David, additional, Frayling, Timothy M, additional, Masoli, Jane AH, additional, Pilling, Luke C, additional, Violán, Concepción, additional, and Delgado, João, additional

Published
2024
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8. Blood Leukocyte DNA Methylation Predicts Risk of Future Myocardial Infarction and Coronary Heart Disease

Author

Agha, Golareh, Mendelson, Michael M, Ward-Caviness, Cavin K, Joehanes, Roby, Huan, TianXiao, Gondalia, Rahul, Salfati, Elias, Brody, Jennifer A, Fiorito, Giovanni, Bressler, Jan, Chen, Brian H, Ligthart, Symen, Guarrera, Simonetta, Colicino, Elena, Just, Allan C, Wahl, Simone, Gieger, Christian, Vandiver, Amy R, Tanaka, Toshiko, Hernandez, Dena G, Pilling, Luke C, Singleton, Andrew B, Sacerdote, Carlotta, Krogh, Vittorio, Panico, Salvatore, Tumino, Rosario, Li, Yun, Zhang, Guosheng, Stewart, James D, Floyd, James S, Wiggins, Kerri L, Rotter, Jerome I, Multhaup, Michael, Bakulski, Kelly, Horvath, Steven, Tsao, Philip S, Absher, Devin M, Vokonas, Pantel, Hirschhorn, Joel, Fallin, M Daniele, Liu, Chunyu, Bandinelli, Stefania, Boerwinkle, Eric, Dehghan, Abbas, Schwartz, Joel D, Psaty, Bruce M, Feinberg, Andrew P, Hou, Lifang, Ferrucci, Luigi, Sotoodehnia, Nona, Matullo, Giuseppe, Peters, Annette, Fornage, Myriam, Assimes, Themistocles L, Whitsel, Eric A, Levy, Daniel, and Baccarelli, Andrea A

Subjects
Human Genome, Heart Disease, Clinical Research, Prevention, Heart Disease - Coronary Heart Disease, Atherosclerosis, Cardiovascular, Genetics, Adult, Aged, Cohort Studies, Coronary Disease, CpG Islands, DNA Methylation, Europe, Female, Genome-Wide Association Study, Humans, Incidence, Leukocytes, Male, Middle Aged, Myocardial Infarction, Population Groups, Prognosis, Prospective Studies, Risk, United States, coronary artery disease, coronary heart disease, epigenetics, genomics, gene expression regulation, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Public Health and Health Services, Cardiovascular System & Hematology
Abstract

BackgroundDNA methylation is implicated in coronary heart disease (CHD), but current evidence is based on small, cross-sectional studies. We examined blood DNA methylation in relation to incident CHD across multiple prospective cohorts.MethodsNine population-based cohorts from the United States and Europe profiled epigenome-wide blood leukocyte DNA methylation using the Illumina Infinium 450k microarray, and prospectively ascertained CHD events including coronary insufficiency/unstable angina, recognized myocardial infarction, coronary revascularization, and coronary death. Cohorts conducted race-specific analyses adjusted for age, sex, smoking, education, body mass index, blood cell type proportions, and technical variables. We conducted fixed-effect meta-analyses across cohorts.ResultsAmong 11 461 individuals (mean age 64 years, 67% women, 35% African American) free of CHD at baseline, 1895 developed CHD during a mean follow-up of 11.2 years. Methylation levels at 52 CpG (cytosine-phosphate-guanine) sites were associated with incident CHD or myocardial infarction (false discovery rate

Published
2019

13. DNA methylation-based measures of biological age: meta-analysis predicting time to death

Author

Chen, Brian H, Marioni, Riccardo E, Colicino, Elena, Peters, Marjolein J, Ward-Caviness, Cavin K, Tsai, Pei-Chien, Roetker, Nicholas S, Just, Allan C, Demerath, Ellen W, Guan, Weihua, Bressler, Jan, Fornage, Myriam, Studenski, Stephanie, Vandiver, Amy R, Moore, Ann Zenobia, Tanaka, Toshiko, Kiel, Douglas P, Liang, Liming, Vokonas, Pantel, Schwartz, Joel, Lunetta, Kathryn L, Murabito, Joanne M, Bandinelli, Stefania, Hernandez, Dena G, Melzer, David, Nalls, Michael, Pilling, Luke C, Price, Timothy R, Singleton, Andrew B, Gieger, Christian, Holle, Rolf, Kretschmer, Anja, Kronenberg, Florian, Kunze, Sonja, Linseisen, Jakob, Meisinger, Christine, Rathmann, Wolfgang, Waldenberger, Melanie, Visscher, Peter M, Shah, Sonia, Wray, Naomi R, McRae, Allan F, Franco, Oscar H, Hofman, Albert, Uitterlinden, André G, Absher, Devin, Assimes, Themistocles, Levine, Morgan E, Lu, Ake T, Tsao, Philip S, Hou, Lifang, Manson, JoAnn E, Carty, Cara L, LaCroix, Andrea Z, Reiner, Alexander P, Spector, Tim D, Feinberg, Andrew P, Levy, Daniel, Baccarelli, Andrea, van Meurs, Joyce, Bell, Jordana T, Peters, Annette, Deary, Ian J, Pankow, James S, Ferrucci, Luigi, and Horvath, Steve

Subjects
Biological Sciences, Genetics, Clinical Research, Prevention, Good Health and Well Being, Aging, DNA Methylation, Epigenesis, Genetic, Female, Humans, Logistic Models, Male, Mortality, Racial Groups, Risk Factors, Survival Analysis, T-Lymphocyte Subsets, all-cause mortality, lifespan, epigenetics, epigenetic clock, DNA methylation, mortality, Biochemistry and cell biology, Clinical sciences
Abstract

Estimates of biological age based on DNA methylation patterns, often referred to as "epigenetic age", "DNAm age", have been shown to be robust biomarkers of age in humans. We previously demonstrated that independent of chronological age, epigenetic age assessed in blood predicted all-cause mortality in four human cohorts. Here, we expanded our original observation to 13 different cohorts for a total sample size of 13,089 individuals, including three racial/ethnic groups. In addition, we examined whether incorporating information on blood cell composition into the epigenetic age metrics improves their predictive power for mortality. All considered measures of epigenetic age acceleration were predictive of mortality (p≤8.2x10-9), independent of chronological age, even after adjusting for additional risk factors (p

Published
2016

17. The transcriptional landscape of age in human peripheral blood.

Author

Peters, Marjolein J, Joehanes, Roby, Pilling, Luke C, Schurmann, Claudia, Conneely, Karen N, Powell, Joseph, Reinmaa, Eva, Sutphin, George L, Zhernakova, Alexandra, Schramm, Katharina, Wilson, Yana A, Kobes, Sayuko, Tukiainen, Taru, NABEC/UKBEC Consortium, Ramos, Yolande F, Göring, Harald HH, Fornage, Myriam, Liu, Yongmei, Gharib, Sina A, Stranger, Barbara E, De Jager, Philip L, Aviv, Abraham, Levy, Daniel, Murabito, Joanne M, Munson, Peter J, Huan, Tianxiao, Hofman, Albert, Uitterlinden, André G, Rivadeneira, Fernando, van Rooij, Jeroen, Stolk, Lisette, Broer, Linda, Verbiest, Michael MPJ, Jhamai, Mila, Arp, Pascal, Metspalu, Andres, Tserel, Liina, Milani, Lili, Samani, Nilesh J, Peterson, Pärt, Kasela, Silva, Codd, Veryan, Peters, Annette, Ward-Caviness, Cavin K, Herder, Christian, Waldenberger, Melanie, Roden, Michael, Singmann, Paula, Zeilinger, Sonja, Illig, Thomas, Homuth, Georg, Grabe, Hans-Jörgen, Völzke, Henry, Steil, Leif, Kocher, Thomas, Murray, Anna, Melzer, David, Yaghootkar, Hanieh, Bandinelli, Stefania, Moses, Eric K, Kent, Jack W, Curran, Joanne E, Johnson, Matthew P, Williams-Blangero, Sarah, Westra, Harm-Jan, McRae, Allan F, Smith, Jennifer A, Kardia, Sharon LR, Hovatta, Iiris, Perola, Markus, Ripatti, Samuli, Salomaa, Veikko, Henders, Anjali K, Martin, Nicholas G, Smith, Alicia K, Mehta, Divya, Binder, Elisabeth B, Nylocks, K Maria, Kennedy, Elizabeth M, Klengel, Torsten, Ding, Jingzhong, Suchy-Dicey, Astrid M, Enquobahrie, Daniel A, Brody, Jennifer, Rotter, Jerome I, Chen, Yii-Der I, Houwing-Duistermaat, Jeanine, Kloppenburg, Margreet, Slagboom, P Eline, Helmer, Quinta, den Hollander, Wouter, Bean, Shannon, Raj, Towfique, Bakhshi, Noman, Wang, Qiao Ping, Oyston, Lisa J, Psaty, Bruce M, Tracy, Russell P, Montgomery, Grant W, and Turner, Stephen T

Subjects
NABEC/UKBEC Consortium, Humans, Gene Expression Profiling, DNA Methylation, Aging, European Continental Ancestry Group, Transcriptome, Biomarkers
Abstract

Disease incidences increase with age, but the molecular characteristics of ageing that lead to increased disease susceptibility remain inadequately understood. Here we perform a whole-blood gene expression meta-analysis in 14,983 individuals of European ancestry (including replication) and identify 1,497 genes that are differentially expressed with chronological age. The age-associated genes do not harbor more age-associated CpG-methylation sites than other genes, but are instead enriched for the presence of potentially functional CpG-methylation sites in enhancer and insulator regions that associate with both chronological age and gene expression levels. We further used the gene expression profiles to calculate the 'transcriptomic age' of an individual, and show that differences between transcriptomic age and chronological age are associated with biological features linked to ageing, such as blood pressure, cholesterol levels, fasting glucose, and body mass index. The transcriptomic prediction model adds biological relevance and complements existing epigenetic prediction models, and can be used by others to calculate transcriptomic age in external cohorts.

Published
2015

18. Human population studies of transcriptome-wide expression in age-related traits

Author

Pilling, Luke C., Melzer, David, Harries, Lorna W., and Studholme, David

Subjects
612.6, Epidemiology, Genomic, Ageing
Abstract

This thesis presents novel investigations of three common ageing phenotypes in human population studies, using microarray technology to assess ‘transcriptome-wide’ expression in whole blood to identify mechanisms and biomarkers. Muscle strength is related to frailty and is predictive of disability in older persons. I assessed the association between transcript abundance in the InCHIANTI peripheral blood samples (N=695) and muscle strength. One gene (CEBPB) passed the multiple testing criteria, and is involved in macrophage-mediated repair of damaged muscle. I extended this work with a meta-analysis of over 7,781 individuals in four collaborating cohorts; expression of over 222 genes were significantly associated with strength, less than half of which have previously been linked to muscle in the literature. CEBPB did not replicate in these younger cohorts. I then performed the first human analysis of gene expression and cognitive function (and separately with decline in cognitive ability over nine years) in the InCHIANTI cohort (N=681), and one gene was identified; CCR2, a chemokine receptor. Evidence in mice has implicated this gene in the accumulation of β-amyloid and cognitive impairment. Finally, in a collaborative project with the Framingham Heart Study I studied age-related inflammation – another hallmark of ageing - using a novel approach to ‘transcriptome-wide’ analysis; each transcript was assessed for the proportion of the association between age and interleukin-6 (IL6) that it statistically mediated. Very few of the genes associated with IL6 alone also mediated the relationship with age. Findings include; SLC4A10, the strongest mediator, not previously linked to inflammation, and interleukin-1 beta and perforin, a cytokine and cytotoxic protein, respectively. These novel analyses highlight key molecular pathways associated with age-related phenotypes in whole blood and provide links between mouse models and humans. They provide biological insight and directions for future research.

Published
2015

19. Genome-wide meta-analysis of muscle weakness identifies 15 susceptibility loci in older men and women

Author

Jones, Garan, Trajanoska, Katerina, Santanasto, Adam J., Stringa, Najada, Kuo, Chia-Ling, Atkins, Janice L., Lewis, Joshua R., Duong, ThuyVy, Hong, Shengjun, Biggs, Mary L., Luan, Jian’an, Sarnowski, Chloe, Lunetta, Kathryn L., Tanaka, Toshiko, Wojczynski, Mary K., Cvejkus, Ryan, Nethander, Maria, Ghasemi, Sahar, Yang, Jingyun, Zillikens, M. Carola, Walter, Stefan, Sicinski, Kamil, Kague, Erika, Ackert-Bicknell, Cheryl L., Arking, Dan E., Windham, B. Gwen, Boerwinkle, Eric, Grove, Megan L., Graff, Misa, Spira, Dominik, Demuth, Ilja, van der Velde, Nathalie, de Groot, Lisette C. P. G. M., Psaty, Bruce M., Odden, Michelle C., Fohner, Alison E., Langenberg, Claudia, Wareham, Nicholas J., Bandinelli, Stefania, van Schoor, Natasja M., Huisman, Martijn, Tan, Qihua, Zmuda, Joseph, Mellström, Dan, Karlsson, Magnus, Bennett, David A., Buchman, Aron S., De Jager, Philip L., Uitterlinden, Andre G., Völker, Uwe, Kocher, Thomas, Teumer, Alexander, Rodriguéz-Mañas, Leocadio, García, Francisco J., Carnicero, José A., Herd, Pamela, Bertram, Lars, Ohlsson, Claes, Murabito, Joanne M., Melzer, David, Kuchel, George A., Ferrucci, Luigi, Karasik, David, Rivadeneira, Fernando, Kiel, Douglas P., and Pilling, Luke C.

Published
2021
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22. A meta-analysis of gene expression signatures of blood pressure and hypertension.

Author

Huan, Tianxiao, Esko, Tõnu, Peters, Marjolein J, Pilling, Luke C, Schramm, Katharina, Schurmann, Claudia, Chen, Brian H, Liu, Chunyu, Joehanes, Roby, Johnson, Andrew D, Yao, Chen, Ying, Sai-Xia, Courchesne, Paul, Milani, Lili, Raghavachari, Nalini, Wang, Richard, Liu, Poching, Reinmaa, Eva, Dehghan, Abbas, Hofman, Albert, Uitterlinden, André G, Hernandez, Dena G, Bandinelli, Stefania, Singleton, Andrew, Melzer, David, Metspalu, Andres, Carstensen, Maren, Grallert, Harald, Herder, Christian, Meitinger, Thomas, Peters, Annette, Roden, Michael, Waldenberger, Melanie, Dörr, Marcus, Felix, Stephan B, Zeller, Tanja, International Consortium for Blood Pressure GWAS (ICBP), Vasan, Ramachandran, O'Donnell, Christopher J, Munson, Peter J, Yang, Xia, Prokisch, Holger, Völker, Uwe, van Meurs, Joyce BJ, Ferrucci, Luigi, and Levy, Daniel

Subjects
International Consortium for Blood Pressure GWAS, Humans, Hypertension, Genetic Predisposition to Disease, Gene Expression Regulation, Blood Pressure, Genotype, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Transcriptome, Cardiovascular, Aging, Genetics, Prevention, Human Genome, Biotechnology, 2.1 Biological and endogenous factors, Developmental Biology
Abstract

Genome-wide association studies (GWAS) have uncovered numerous genetic variants (SNPs) that are associated with blood pressure (BP). Genetic variants may lead to BP changes by acting on intermediate molecular phenotypes such as coded protein sequence or gene expression, which in turn affect BP variability. Therefore, characterizing genes whose expression is associated with BP may reveal cellular processes involved in BP regulation and uncover how transcripts mediate genetic and environmental effects on BP variability. A meta-analysis of results from six studies of global gene expression profiles of BP and hypertension in whole blood was performed in 7017 individuals who were not receiving antihypertensive drug treatment. We identified 34 genes that were differentially expressed in relation to BP (Bonferroni-corrected p

Published
2015

24. Does physical activity moderate the association between shorter leukocyte telomere length and incident coronary heart disease? Data from 54,180 UK Biobank participants

Author

Xiang, Meiruo, primary, Pilling, Luke C., additional, Melzer, David, additional, Kirk, Ben, additional, Duque, Gustavo, additional, Liu, Rui, additional, Kuchel, George A., additional, Wood, Andrew R., additional, Metcalf, Brad, additional, Diniz, Breno S., additional, Hillsdon, Melvyn, additional, and Kuo, Chia-Ling, additional

Published
2023
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26. A Genome-Wide Association Study of Depressive Symptoms

Author

Hek, Karin, Demirkan, Ayse, Lahti, Jari, Terracciano, Antonio, Teumer, Alexander, Cornelis, Marilyn C, Amin, Najaf, Bakshis, Erin, Baumert, Jens, Ding, Jingzhong, Liu, Yongmei, Marciante, Kristin, Meirelles, Osorio, Nalls, Michael A, Sun, Yan V, Vogelzangs, Nicole, Yu, Lei, Bandinelli, Stefania, Benjamin, Emelia J, Bennett, David A, Boomsma, Dorret, Cannas, Alessandra, Coker, Laura H, de Geus, Eco, De Jager, Philip L, Diez-Roux, Ana V, Purcell, Shaun, Hu, Frank B, Rimm, Eric B, Hunter, David J, Jensen, Majken K, Curhan, Gary, Rice, Kenneth, Penman, Alan D, Rotter, Jerome I, Sotoodehnia, Nona, Emeny, Rebecca, Eriksson, Johan G, Evans, Denis A, Ferrucci, Luigi, Fornage, Myriam, Gudnason, Vilmundur, Hofman, Albert, Illig, Thomas, Kardia, Sharon, Kelly-Hayes, Margaret, Koenen, Karestan, Kraft, Peter, Kuningas, Maris, Massaro, Joseph M, Melzer, David, Mulas, Antonella, Mulder, Cornelis L, Murray, Anna, Oostra, Ben A, Palotie, Aarno, Penninx, Brenda, Petersmann, Astrid, Pilling, Luke C, Psaty, Bruce, Rawal, Rajesh, Reiman, Eric M, Schulz, Andrea, Shulman, Joshua M, Singleton, Andrew B, Smith, Albert V, Sutin, Angelina R, Uitterlinden, André G, Völzke, Henry, Widen, Elisabeth, Yaffe, Kristine, Zonderman, Alan B, Cucca, Francesco, Harris, Tamara, Ladwig, Karl-Heinz, Llewellyn, David J, Räikkönen, Katri, Tanaka, Toshiko, van Duijn, Cornelia M, Grabe, Hans J, Launer, Lenore J, Lunetta, Kathryn L, Mosley, Thomas H, Newman, Anne B, Tiemeier, Henning, and Murabito, Joanne

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Behavioral and Social Science, Depression, Brain Disorders, Human Genome, Mental Health, 2.1 Biological and endogenous factors, Aetiology, Aged, Aged, 80 and over, Chromosomes, Human, Pair 5, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Center for Epidemiologic Studies Depression Scale, CHARGE consortium, depression, depressive symptoms, genetics, genome-wide association study, meta-analysis, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Biological sciences, Biomedical and clinical sciences, Psychology
Abstract

BackgroundDepression is a heritable trait that exists on a continuum of varying severity and duration. Yet, the search for genetic variants associated with depression has had few successes. We exploit the entire continuum of depression to find common variants for depressive symptoms.MethodsIn this genome-wide association study, we combined the results of 17 population-based studies assessing depressive symptoms with the Center for Epidemiological Studies Depression Scale. Replication of the independent top hits (p

Published
2013

27. Mid‐life leukocyte telomere length and dementia risk: An observational and mendelian randomization study of 435,046 UK Biobank participants

Author

Liu, Rui, primary, Xiang, Meiruo, additional, Pilling, Luke C., additional, Melzer, David, additional, Wang, Lihong, additional, Manning, Kevin J., additional, Steffens, David C., additional, Bowden, Jack, additional, Fortinsky, Richard H., additional, Kuchel, George A., additional, Rhee, Taeho G., additional, Diniz, Breno S., additional, and Kuo, Chia‐Ling, additional

Published
2023
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38. Mid-life leukocyte telomere length and dementia risk: a prospective cohort study of 435,046 UK Biobank participants

Author

Liu, Rui, primary, Xiang, Meiruo, additional, Pilling, Luke C., additional, Melzer, David, additional, Wang, Lihong, additional, Manning, Kevin J., additional, Steffens, David C., additional, Bowden, Jack, additional, Fortinsky, Richard H., additional, Kuchel, George A., additional, Rhee, Taeho G, additional, Diniz, Breno S., additional, and Kuo, Chia-Ling, additional

Published
2022
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42. Additional file 1 of Heavy-load exercise in older adults activates vasculogenesis and has a stronger impact on muscle gene expression than in young adults

Author

Gautvik, Kaare M., Olstad, Ole K., Raue, Ulrika, Gautvik, Vigdis T., Kvernevik, Karl J., Utheim, Tor P., Ravnum, Solveig, Kirkegaard, Camilla, Wiig, Håvard, Jones, Garan, Pilling, Luke C., Trappe, Scott, Raastad, Truls, and Reppe, Sjur

Abstract

Addiitional file 1: Figure S1. Comparison of transcript signal levels between os ilium–associated muscle and thigh muscle. Figure S2. Genes within the Diseases and Function category Vasculogenesis with increased (red) or reduced (green) expression end vs start of the training period in elderly as compared to young. Table S1. Common annotated genes changed in elderly in both Oslo and BSU cohorts at Q-value

Published
2022
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43. Calcium‐channel blockers: Clinical outcome associations with reported pharmacogenetics variants in 32 000 patients.

Author

Türkmen, Deniz, Masoli, Jane A. H., Delgado, João, Kuo, Chia‐Ling, Bowden, Jack, Melzer, David, and Pilling, Luke C.

Subjects
PHARMACOGENOMICS, TREATMENT effectiveness, CORONARY disease, GENETIC variation, CARDIAC patients
Abstract

Aims: Pharmacogenetic variants impact dihydropyridine calcium‐channel blockers (dCCBs; e.g., amlodipine) treatment efficacy, yet evidence on clinical outcomes in routine primary care is limited. Reported associations in pharmacogenomics knowledge base PharmGKB have weak supporting evidence. We aimed to estimate associations between reported pharmacogenetic variants and incident adverse events in a community‐based cohort prescribed dCCB. Methods: We analysed up to 32 360 UK Biobank participants prescribed dCCB in primary care (from UK general practices, 1990–2017). We investigated 23 genetic variants. Outcomes were incident diagnosis of coronary heart disease, heart failure (HF), chronic kidney disease, oedema and switching antihypertensive medication. Results: Participants were aged 40–79 years at first dCCB prescription. Carriers of rs877087 T allele in RYR3 had increased risk of hazard ratio (HF 1.13: 95% confidence interval 1.02 to 1.25, P =.02). Although nonsignificant after multiple testing correction, the association is consistent with prior evidence. We estimated that if rs877087 T allele could experience the same treatment effect as noncarriers, the incidence of HF in patients prescribed dCCB would reduce by 9.2% (95% confidence interval 3.1 to 15.4). In patients with a history of heart disease prior to dCCB (n = 2296), rs877087 homozygotes had increased risk of new coronary heart disease or HF compared to CC variant. rs10898815 in NUMA1 and rs776746 in CYP3A5 increased likelihood of switching to an alternative antihypertensive. The remaining variants were not strongly or consistently associated with studied outcomes. Conclusion: Patients with common genetic variants in NUMA1, CYP3A5 and RYR3 had increased adverse clinical outcomes. Work is needed to establish whether outcomes of dCCB prescribing could be improved by prior knowledge of pharmacogenetics variants supported by clinical evidence of association with adverse events. [ABSTRACT FROM AUTHOR]

Published
2023
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50. Analysis ofCYP2C19genetic variants with ischaemic events in UK patients prescribed clopidogrel in primary care: a retrospective cohort study

Author

Pilling, Luke C, primary, Türkmen, Deniz, additional, Fullalove, Hannah, additional, Atkins, Janice L, additional, Delgado, Joao, additional, Kuo, Chia-Ling, additional, Kuchel, George A, additional, Ferrucci, Luigi, additional, Bowden, Jack, additional, Masoli, Jane A H, additional, and Melzer, David, additional

Published
2021
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