- Member of the British Society for Genetic Medicine (BSGM)
- Member of the Clinical Genetic Science (ACGS)
Nadia’s work in Translational Medicine Research thus far focuses on the discovery of novel disease-related genes/metabolites helping people to prevent or treat that disease.
As a Post-Doctoral Research Fellow in the Antoniades group, Nadia’s main project is to process, analyse and interpret the raw data generated from various genetic tools investigating the signalling pathways orchestrating the crosstalk between adipose tissue and cardiovascular system. The main aim of this project is to identify the pathways and biological processes most affected in the datasets and point out the key players in the cardiovascular pathogenesis as potential drug targets and/or disease biomarkers. Part of her role in this project is to carry out some specialised cellular and molecular experiments in the labs to validate the newly identified candidates.
Nadia also assists the team with the processing and interpretation of their raw data from various translational research projects in cardiovascular and related diseases to identify clinically relevant perturbations and their possible culprits.
Nadia completed her PhD by the end of 2013 in Clinical Genetics at the College of Medicine and Health Sciences-United Arab Emirates University. While there, she studied the Genome of several families with genetic diseases revealing their underlying genetic abnormalities and molecular/cellular pathogenesis.
Nadia joined the Hurles group at the Wellcome Trust Sanger Institute in 2014 as a member of the analysis team of the Deciphering Developmental Disorders project. Nadia has applied her knowledge of clinical genetics and development to discover novel disease genes underlying developmental disorders. During her employment at the Sanger Institute, she analysed the exomes of more than 4000 patients with developmental disorders and discovered several novel disease-causing genes and their possible pathophysiology.
Insulin-induced vascular redox dysregulation in human atherosclerosis is ameliorated by dipeptidyl peptidase 4 inhibition.
Akoumianakis I. et al, (2020), Sci Transl Med, 12
Wnt5a contributes to human atherosclerosis via novel USP17 redox signalling
Akoumianakis I. et al, (2019), EUROPEAN HEART JOURNAL, 40, 1660 - 1660