Fabiola Del Greco M

ORCID: 0009-0007-0023-6901
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About
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Research Areas
  • Genetic Associations and Epidemiology
  • Genetic and phenotypic traits in livestock
  • Genetic Mapping and Diversity in Plants and Animals
  • Folate and B Vitamins Research
  • Birth, Development, and Health
  • Cardiac electrophysiology and arrhythmias
  • Metabolomics and Mass Spectrometry Studies
  • Liver Disease Diagnosis and Treatment
  • Parkinson's Disease Mechanisms and Treatments
  • Hormonal Regulation and Hypertension
  • Bioinformatics and Genomic Networks
  • Nutrition, Genetics, and Disease
  • Adipokines, Inflammation, and Metabolic Diseases
  • Iron Metabolism and Disorders
  • Thyroid Disorders and Treatments
  • Growth Hormone and Insulin-like Growth Factors
  • Diet, Metabolism, and Disease
  • Health, Environment, Cognitive Aging
  • Genetics and Neurodevelopmental Disorders
  • Sleep and related disorders
  • Adipose Tissue and Metabolism
  • Renin-Angiotensin System Studies
  • Ion channel regulation and function
  • Pesticide Exposure and Toxicity
  • Molecular Biology Techniques and Applications

Institute for Biomedicine
2015-2024

Eurac Research
2015-2024

University of Lübeck
2011-2022

Leiden University Medical Center
2021

Leiden University
2021

University Hospital Schleswig-Holstein
2019

Imperial College Healthcare NHS Trust
2017

University College London
2017

Imperial College London
2013-2017

Erasmus MC
2017

Mendelian randomization (MR) uses genetic data to probe questions of causality in epidemiological research, by invoking the Instrumental Variable (IV) assumptions. In recent years, it has become commonplace attempt MR analyses synthesising summary estimates association gleaned from large and independent study populations. This is referred as two‐sample MR. Unfortunately, due sheer number variants that can be easily included into analyses, increasingly likely some do not meet IV assumptions...

10.1002/sim.7221 article EN cc-by Statistics in Medicine 2017-01-23

Background: MR-Egger regression has recently been proposed as a method for Mendelian randomization (MR) analyses incorporating summary data estimates of causal effect from multiple individual variants, which is robust to invalid instruments. It can be used test directional pleiotropy and provides an estimate the adjusted its presence. useful additional sensitivity analysis standard inverse variance weighted (IVW) approach that assumes all variants are valid Both methods use weights consider...

10.1093/ije/dyw220 article EN cc-by International Journal of Epidemiology 2016-09-11

Mendelian randomisation (MR) estimates causal effects of modifiable phenotypes on an outcome by using genetic variants as instrumental variables, but its validity relies the assumption no pleiotropy, that is, genes influence only through given phenotype. Excluding pleiotropy is difficult, use multiple instruments can indirectly address issue: if all represent valid instruments, their MR should vary chance. The Sargan test detects when individual phenotype, and genotype data are measured in...

10.1002/sim.6522 article EN Statistics in Medicine 2015-05-07

data furnishing a two-sample Mendelian randomization (MR) study are often visualized with the aid of scatter plot, in which single-nucleotide polymorphism (SNP)-outcome associations plotted against SNP-exposure to provide an immediate picture causal-effect estimate for each individual variant. It is also convenient overlay standard inverse-variance weighted (IVW) causal effect as fitted slope, see whether SNP provides evidence that supports, or conflicts with, overall consensus....

10.1093/ije/dyy101 article EN cc-by International Journal of Epidemiology 2018-05-14

Two-sample summary-data Mendelian randomization (MR) incorporating multiple genetic variants within a meta-analysis framework is popular technique for assessing causality in epidemiology. If all satisfy the instrumental variable (IV) and necessary modelling assumptions, then their individual ratio estimates of causal effect should be homogeneous. Observed heterogeneity signals that one or more these assumptions could have been violated.Causal estimation assessment MR require an approximation...

10.1093/ije/dyy258 article EN cc-by International Journal of Epidemiology 2018-11-15

Abstract Background With genome-wide association data for many exposures and outcomes now available from large biobanks, one-sample Mendelian randomization (MR) is increasingly used to investigate causal relationships. Many robust MR methods are address pleiotropy, but these assume independence between the gene-exposure gene-outcome estimates. Unlike in two-sample MR, two estimates obtained same individuals, assumption of does not hold presence confounding. Methods simulations mimicking a...

10.1093/ije/dyab084 article EN cc-by International Journal of Epidemiology 2021-04-06
Tuomas O. Kilpeläinen Jayne F. Martin Carli Alicja A. Skowronski Qi Sun Jennifer Kriebel and 95 more Mary F. Feitosa Åsa K. Hedman Alexander Drong James E. Hayes Jinghua Zhao Tune H. Pers Ursula M. Schick Niels Grarup Zoltán Kutalik Stella Trompet Massimo Mangino Kati Kristiansson Marian Beekman Leo‐Pekka Lyytikäinen Joel Eriksson Peter Henneman Jari Lahti Toshiko Tanaka Jian’an Luan Fabiola Del Greco M Dorota Pasko Frida Renström Sara M. Willems Anubha Mahajan Lynda M. Rose Xiuqing Guo Yongmei Liu Marcus E. Kleber Louis Pérusse Tom R. Gaunt Tarunveer S. Ahluwalia Yan V. Sun Y.F. Ramos Najaf Amin Antoinette Amuzu Inês Barroso Claire Bellis John Blangero Brendan M. Buckley Stefan Böhringer Yii‐Der I. Chen Anton J. N. de Craen David R. Crosslin Caroline Dale Zari Dastani Felix R. Day Joris Deelen Graciela E. Delgado Ayşe Demirkan Francis Finucane Ian Ford Melissa E. Garcia Christian Gieger Stefan Gustafsson Göran Hallmans Susan E. Hankinson Aki S. Havulinna Christian Herder Dena Hernandez Andrew A. Hicks David J. Hunter Thomas Illig Erik Ingelsson Andreea Ioan‐Facsinay John‐Olov Jansson Nancy S. Jenny Marit E. Jørgensen Torben Jørgensen Magnus K. Karlsson Wolfgang Köenig Peter Kraft Joanneke C. Kwekkeboom Tiina Laatikainen Karl‐Heinz Ladwig Charles A. LeDuc Gordon Lowe Yingchang Lu Pedro Marques‐Vidal Christa Meisinger Cristina Menni Andrew P. Morris Richard H. Myers Satu Männistö Mike A. Nalls Lavinia Paternoster Annette Peters Aruna D. Pradhan Tuomo Rankinen Laura J. Rasmussen‐Torvik Wolfgang Rathmann Treva Rice J. Brent Richards Paul M. Ridker Naveed Sattar David B. Savage

Abstract Leptin is an adipocyte-secreted hormone, the circulating levels of which correlate closely with overall adiposity. Although rare mutations in leptin ( LEP ) gene are well known to cause deficiency and severe obesity, no common loci regulating have been uncovered. Therefore, we performed a genome-wide association study (GWAS) from 32,161 individuals followed up reaching P <10 −6 19,979 additional individuals. We identify five robustly associated <5 × 10 −8 in/near , SLC32A1...

10.1038/ncomms10494 article EN cc-by Nature Communications 2016-02-01

Although levels of iron are known to be increased in the brains patients with Parkinson disease (PD), epidemiological evidence on a possible effect blood PD risk is inconclusive, effects reported opposite directions. Epidemiological studies suffer from problems confounding and reverse causation, mendelian randomization (MR) represents an alternative approach provide unconfounded estimates biomarkers disease. We performed MR study where genes modify were used as instruments estimate risk,...

10.1371/journal.pmed.1001462 article EN cc-by PLoS Medicine 2013-06-04
Louise V. Wain Ahmad Vaez Rick Jansen Roby Joehanes Peter J. van der Most and 95 more A. Mesut Erzurumluoglu Paul F. O’Reilly Claudia P. Cabrera Helen R. Warren Lynda M. Rose Germaine C. Verwoert Jouke‐Jan Hottenga Rona J. Strawbridge Tõnu Esko Dan E. Arking Shih-Jen Hwang Xiuqing Guo Zoltán Kutalik Stella Trompet Nick Shrine Alexander Teumer Janina S. Ried Joshua C. Bis Albert V. Smith Najaf Amin Ilja M. Nolte Leo‐Pekka Lyytikäinen Anubha Mahajan Nicholas J. Wareham Edith Hofer Peter K. Joshi Kati Kristiansson Michela Traglia Aki S. Havulinna Anuj Goel Mike A. Nalls Siim Sõber Dragana Vuckovic Jian’an Luan Fabiola Del Greco M Kristin L. Ayers Jaume Marrugat Daniela Ruggiero Lorna M. Lopez Teemu Niiranen Stefan Enroth Anne Jackson Christopher P. Nelson Jennifer E. Huffman Weihua Zhang Jonathan Marten Ilaria Gandin Sarah E. Harris Tatijana Zemunik Yingchang Lu Εvangelos Εvangelou Nabi Shah Martin H. de Borst Massimo Mangino Bram P. Prins Archie Campbell Ruifang Li‐Gao Ganesh Chauhan Christopher Oldmeadow Gonçalo Abecasis Maryam Abedi Caterina Barbieri Michael R. Barnes Chiara Batini John Beilby Tineka Blake Michael Boehnke Erwin P. Böttinger Peter S. Braund Morris J. Brown Marco Brumat Harry Campbell John C. Chambers Massimiliano Cocca Francis S. Collins John Connell Heather J. Cordell Jeffrey Damman Gail Davies Eco J. C. de Geus Renée de Mutsert Joris Deelen Yusuf Demirkale Alex S. F. Doney Marcus Dörr Martin Farrall Teresa Ferreira Mattias Frånberg He Gao Vilmantas Giedraitis Christian Gieger Franco Giulianini Alan J. Gow Anders Hamsten Tamara B. Harris

Elevated blood pressure is a major risk factor for cardiovascular disease and has substantial genetic contribution. Genetic variation influencing the potential to identify new pharmacological targets treatment of hypertension. To discover additional novel loci, we used 1000 Genomes Project–based imputation in 150 134 European ancestry individuals sought significant evidence independent replication further 228 245 individuals. We report 6 signals association or near HSPB7 , TNXB LRP12...

10.1161/hypertensionaha.117.09438 article EN Hypertension 2017-07-25
Pim van der Harst Jessica van Setten Niek Verweij Georg Vogler Lude Franke and 95 more Matthew T. Maurano Xinchen Wang Irene Mateo Leach Mark Eijgelsheim Nona Sotoodehnia Caroline Hayward Rossella Sorice Osorio Meirelles Leo‐Pekka Lyytikäinen Ozren Polašek Toshiko Tanaka Dan E. Arking Sheila Ulivi Stella Trompet Martina Müller‐Nurasyid Albert V. Smith Marcus Dörr Kathleen F. Kerr Jared W. Magnani Fabiola Del Greco M Weihua Zhang Ilja M. Nolte Claudia Silva Sandosh Padmanabhan Vinicius Tragante Tõnu Esko Gonçalo R. Abecasis Michiel Adriaens Karl Andersen Phil Barnett Joshua C. Bis Rolf Bodmer Brendan M. Buckley Harry Campbell Megan V. Cannon Aravinda Chakravarti Lin Y. Chen Alessandro Delitala Richard B. Devereux Pieter A. Doevendans Anna F. Dominiczak Luigi Ferrucci Ian Ford Christian Gieger Tamara B. Harris Eric Haugen Matthias Heinig Dena Hernandez Hans L. Hillege Joel N. Hirschhorn Albert Hofman Norbert Hübner Shih-Jen Hwang Alfonso Iorio Mika Kähönen Manolis Kellis Ivana Kolčić Ishminder K. Kooner Jaspal S. Kooner Jan A. Kors Edward G. Lakatta Kasper Lage Lenore J. Launer Daniel Levy Alicia Lundby Peter W. Macfarlane Dalit May Thomas Meitinger Andres Metspalu Stefania Nappo Silvia Naitza Shane Neph Alex S. Nord Teresa Nutile Peter M. Okin Jesper V. Olsen Ben A. Oostra Josef Penninger L Pennacchio Tune H. Pers Siegfried Perz Annette Peters Yigal M. Pinto Arne Pfeufer Maria Grazia Pilia Peter P. Pramstaller Bram P. Prins Olli T. Raitakari Soumya Raychaudhuri Kenneth Rice Elizabeth J. Rossin Jerome I. Rotter Sebastian Schäfer David Schlessinger Carsten Oliver Schmidt

Myocardial mass is a key determinant of cardiac muscle function and hypertrophy. depolarization leading to contraction reflected by the amplitude duration QRS complex on electrocardiogram (ECG). Abnormal or reflect changes in myocardial conduction, are associated with increased risk heart failure death. This meta-analysis sought gain insights into genetic determinants mass. We carried out genome-wide association 4 traits up 73,518 individuals European ancestry, followed extensive biological...

10.1016/j.jacc.2016.07.729 article EN cc-by-nc-nd Journal of the American College of Cardiology 2016-09-01
Philipp S. Wild Janine F. Felix Arne Schillert Alexander Teumer Ming‐Huei Chen and 95 more Maarten J.G. Leening Uwe Völker Vera Großmann Jennifer A. Brody Marguerite R. Irvin Sanjiv J. Shah Setia Pramana Wolfgang Lieb Reinhold Schmidt Alice Stanton Dörthe Malzahn Albert V. Smith Johan Sundström Cosetta Minelli Daniela Ruggiero Leo‐Pekka Lyytikäinen Daniel Tiller J. G. Smith Claire Monnereau Marco R. Di Tullio Solomon K. Musani Alanna C. Morrison Tune H. Pers Michael P. Morley Marcus E. Kleber Jayashri Aragam Emelia J. Benjamin Joshua C. Bis Egbert Bisping Ulrich Broeckel Susan Cheng Jaap W. Deckers Fabiola Del Greco M Frank Edelmann Myriam Fornage Lude Franke Nele Friedrich Tamara B. Harris Edith Hofer Albert Hofman Jie Huang Alun D. Hughes Mika Kähönen KNHI investigators Jochen Kruppa Karl J. Lackner Lars Lannfelt Rafael Laskowski Lenore J. Launer Margrét Leósdóttir Honghuang Lin Cecilia M. Lindgren Christina Loley Calum A. MacRae Deborah Mascalzoni Jamil Mayet Daniel Medenwald Andrew P. Morris Christian Müller Martina Müller‐Nurasyid Stefania Nappo Peter M. Nilsson Sebastian Nuding Teresa Nutile Annette Peters Arne Pfeufer Diana Pietzner Peter P. Pramstaller Olli T. Raitakari Kenneth Rice Fernando Rivadeneira Jerome I. Rotter Saku Ruohonen Ralph L. Sacco Tandaw E. Samdarshi Helena Schmidt Andrew Sharp Denis C. Shields Rossella Sorice Nona Sotoodehnia Bruno H. Stricker Praveen Surendran Simon Thom Anna Maria Töglhofer André G. Uitterlinden Rolf Wachter Henry Völzke Andreas Ziegler Thomas Münzel Winfried März Thomas P. Cappola Joel N. Hirschhorn Gary F. Mitchell Nicholas L. Smith Ervin R. Fox

Understanding the genetic architecture of cardiac structure and function may help to prevent treat heart disease. This investigation sought identify common variations associated with inter-individual variability in function.

10.1172/jci84840 article EN Journal of Clinical Investigation 2017-04-09

10.1007/978-1-4939-7274-6_29 article EN Methods in molecular biology 2017-01-01

Mitochondria play an important role in cellular metabolism, and their dysfunction is postulated to be involved metabolic disturbances. Mitochondrial DNA present multiple copies per cell. The quantification of mitochondrial copy number (mtDNA-CN) might used assess dysfunction.

10.1111/joim.13242 article EN cc-by Journal of Internal Medicine 2021-01-16

Abstract There is increasing evidence for inflammation as a determinant in the pathogenesis of Parkinson’s disease, but its role parkinsonian neurodegeneration remains elusive. It not clear whether inflammatory cascades are causes or consequences dopamine neuron death. In present study, we aim to perform an in-depth statistical investigation causal relationship between and disease using two-sample Mendelian randomization design. Genetic instruments were selected summary-level data from...

10.1093/brain/awac193 article EN cc-by-nc Brain 2022-06-03
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