Publications by authors named "Eleni Friligkou"
This study explores the genetic and epidemiologic correlates of long-term photoplethysmography-derived pulse rate variability (PRV) measurements with anxiety disorders. Individuals with whole-genome sequencing, Fitbit, and electronic health record data (N = 920; 61,333 data points) were selected from the All of Us Research Program. Anxiety polygenic risk scores (PRS) were derived with PRS-CS after meta-analyzing anxiety genome-wide association studies from three major cohorts- UK Biobank, FinnGen, and the Million Veterans Program (N =364,550).
View Article and Find Full Text PDFObjective: This study investigated the genetic and epigenetic mechanisms underlying the comorbidity patterns of five substance dependence diagnoses (SDs; alcohol, AD; cannabis, CaD; cocaine, CoD; opioid, OD; tobacco, TD).
Methods: A latent class analysis (LCA) was performed on 31,197 individuals (average age 42±11 years; 49% females) from six cohorts to identify comorbid DSM-IV SD patterns. In subsets of this sample, we tested SD-latent classes with respect to polygenic burden of psychiatric and behavioral traits and epigenome-wide changes in three population groups.
Article Synopsis
- * Polygenic risk scores from European individuals were found to correlate with anxiety in other groups, including African and East Asian populations, indicating shared genetic factors.
- * The study revealed that anxiety is linked to specific brain areas and has genetic ties to other mental health conditions, underscoring the need for diverse population research and multi-omics approaches.
Background: Patients with post-traumatic stress disorder (PTSD) experience higher risk of adverse cardiovascular (CV) outcomes. This study explores shared loci, and genes between PTSD and CV conditions from three major domains: CV diagnoses from electronic health records (CV-EHR), cardiac and aortic imaging, and CV health behaviors defined in Life's Essential 8 (LE8).
Methods: We used genome-wide association study (GWAS) of PTSD (N=1,222,882), 246 CV diagnoses based on EHR data from Million Veteran Program (MVP; N=458,061), UK Biobank (UKBB; N=420,531), 82 cardiac and aortic imaging traits (N=26,893), and GWAS of traits defined in the LE8 (N = 282,271 ~ 1,320,016).
Introduction: While higher socioeconomic factors (SEF) and cognitive performance (CP) have been associated with reduced Alzheimer's disease (AD) risk, recent evidence highlighted that these factors may have opposite effects on family history of AD (FHAD).
Methods: Leveraging data from the UK Biobank (N=448,100) and the All of Us Research Program (N=240,319), we applied generalized linear regression models, polygenic risk scoring (PRS), and one-sample Mendelian randomization (MR) to test the sex-specific SEF and CP associations with AD and FHAD.
Results: Observational and genetically informed analyses highlighted that higher SEF and CP were associated with reduced AD and sibling-FHAD, while these factors were associated with increased parent-FHAD.
What distinguishes vulnerability and resilience to posttraumatic stress disorder (PTSD) remains unclear. Levering traumatic experiences reporting, genetic data, and electronic health records (EHR), we investigated and predicted the clinical comorbidities (co-phenome) of PTSD vulnerability and resilience in the UK Biobank (UKB) and All of Us Research Program (AoU), respectively. In 60,354 trauma-exposed UKB participants, we defined PTSD vulnerability and resilience considering PTSD symptoms, trauma burden, and polygenic risk scores.
View Article and Find Full Text PDFArticle Synopsis
- * Polygenic risk scores from European individuals showed links to anxiety in diverse groups like African and East Asian populations, indicating the genetic factors may be shared across ancestries.
- * The study found higher heritability of anxiety linked to brain regions involved in emotion and cognition, along with relationships to other mental health disorders and some physical health issues, emphasizing the need for diverse population analyses and comprehensive genetic approaches.
Individuals suffering from chronic pain develop substance use disorders (SUDs) more often than others. Understanding the shared genetic influences underlying the comorbidity between chronic pain and SUDs will lead to a greater understanding of their biology. Genome-wide association statistics were obtained from the UK Biobank for multisite chronic pain (MCP, N = 387,649) and from the Million Veteran Program and the Psychiatric Genomics Consortium meta-analyses for alcohol use disorder (AUD, N = 296,974), cannabis use disorder (CanUD, N = 161,053), opioid use disorder (OUD, N = 57,120), and problematic tobacco use (PTU, N = 270,120).
View Article and Find Full Text PDFArticle Synopsis
- Researchers examined how ADHD relates genetically to various substance use disorders (SUDs) using data from large genome-wide association studies (GWAS).
- They found strong genetic correlations between ADHD and SUDs like cannabis and opioid use disorder, as well as problematic alcohol and tobacco use, with a notable pleiotropic SNP indicating shared genetic factors.
- The study suggests that SUDs, particularly problematic alcohol and tobacco use, have a stronger causal effect on ADHD than vice versa, highlighting complex genetic links and shared risk factors contributing to their comorbidity.
Background: To gain insights into the role of brain structure and function on anxiety (ANX), we conducted a genetically informed investigation leveraging information from ANX genome-wide association studies available from the UK Biobank (n = 380,379), the FinnGen Program (n = 290,361), and the Million Veteran Program (n = 175,163) together with UK Biobank genome-wide data (n = 33,224) related to 3935 brain imaging-derived phenotypes (IDPs).
Methods: A genetic correlation analysis between ANX and brain IDPs was performed using linkage disequilibrium score regression. To investigate ANX-brain associations, a 2-sample Mendelian randomization was performed considering multiple methods and sensitivity analyses.
Background: To gain insights into the role of brain structure and function on anxiety (ANX), we conducted a genetically informed investigation leveraging information from ANX genome-wide association studies available from UK Biobank (UKB; N=380,379), FinnGen Program (N=290,361), and Million Veteran Program (MVP; N=199,611) together with UKB genome-wide data (N=33,224) related to 3,935 brain imaging-derived phenotypes (IDP).
Methods: A genetic correlation analysis between ANX and brain IDPs was performed using linkage disequilibrium score regression. To investigate ANX-brain associations, a two-sample Mendelian randomization (MR) was performed considering multiple methods and sensitivity analyses.
Background: Anxiety disorders are associated with decreased heart rate variability (HRV), but the underlying mechanisms remain elusive.
Methods: We selected individuals with whole-genome sequencing, Fitbit, and electronic health record data (N=920; 61,333 data points) from the All of Us Research Program. Anxiety PRS were derived with PRS-CS after meta-analyzing anxiety genome-wide association studies from three major cohorts-UK Biobank, FinnGen, and the Million Veterans Program (N Total =364,550).