Congratulations to Chen-Yang Su, PhD student of the McGill CERC in Genomic Medicine for winning the Trainee Poster Excellence Award at the 1st Canadian Symposium on Long COVID on Sep 20-21, 2023 !
You will find the abstract of his poster below:
Combining proteomics and metabolomics to identify signatures protective of neurological consequences of post-acute SARS-CoV-2 infection.
Chen-Yang Su1,3*, Sirui Zhou2,3*
Introduction: Post-acute sequelae SARS-CoV-2 (PASC) has heterogeneous manifestations including debilitating long-term neurological symptoms.
Methods: We measured 4,984 proteins and 943 metabolites in 1,234 individuals from the Biobanque Québécoise de la COVID-19 (BQC19). Using 689 clinical entries, we defined Broad Neurological PASC (BNP) as any neurological manifestations and Refined Neurological PASC (RNP) as neurological complications that recently appeared or deteriorated due to COVID-19. We fitted single-biomarker logistic regression models adjusting for age and sex to determine the association of each biomarker with PASC outcomes.
Results: We compared 381 BNP and 65 RNP cases with both proteomics and metabolomics data with 535 and 713 controls, respectively. We found 1,416 and 734 proteins significantly associated with BNP and RNP, respectively, with 544 overlapping proteins. For metabolites, 158 and 130 were significantly associated with BNP and RNP, respectively, with 53 overlapping. We identified phosphatidylethanolamine-binding protein 1 (PEBP1) as being protective against BNP (OR: 0.76 (0.66-0.87), FDR p: 0.002) and RNP (OR: 0.61 (0.46-0.81), FDR p: 0.014). Interestingly, previous studies suggested downregulation of PEBP1 may lead to Alzheimer’s disease. Moreover, PEBP1 is an enzyme for 1-palmitoyl-2-docosahexaenoyl-GPE, a phosphatidylethanolamine (PE) whose impairment leads to neurodegenerative disorders, which is concordant with our finding that increased circulating PE is associated with decreased neurological PASC risk (BNP OR: 0.78 (0.68-0.90), FDR p: 0.01; RNP OR: 0.56 (0.41-0.75), FDR p: 0.006).
Conclusion: We used an integrative bi-omics approach to provide new insight into the pathophysiological mechanisms underlying neurological PASC risk which may point to new ways to treat this condition.