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Bru Cormand

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Articles

Multi-ancestry genome-wide association and integrated multi-omics analyses of endometriosis and its clinical manifestations

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By Dora Koller, Jun He, Solveig Løkhammer, Dan Qiu, David Davtian, Qianyu Chen, Ziang Xu, Zhongzheng Mao, Eleni Friligkou, Bru Cormand, Idhaliz Flores, Signe Altmae, Signe Altmäe, Marina Mitjans, Brenda Cabrera-Mendoza, Renato Polimanti, Selena Aranda, Sefayet Karaca
| Nature Verified
Abstract Endometriosis is a chronic systemic disease affecting ~10% of women, yet its genetic basis and molecular mechanisms remain poorly understood. Hence, here we conducted a genome-wide association study of endometriosis and adenomyosis in ~1.4 million women, including 105,869 cases, aiming to expand loci discovery across ancestries, dissect symptom-specific effects and integrate multi-omic data.
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rbfox1 LoF mutants show disrupted bdnf/trkb2 and crhb/nr3c2 expression and increased cortisol levels during development coupled with signs of allostatic overload in adulthood | Translational Psychiatry

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By Adele Leggieri, Judit García-González, Peter Ashdown, Bru Cormand
| Nature Verified
Abstract Mutations in the RBFOX1 gene are associated with psychiatric disorders but how RBFOX1 influences psychiatric disorder vulnerability remains unclear. Recent studies showed that RBFOX proteins mediate the alternative splicing of PAC1, a critical HPA axis activator. Further, RBFOX1 dysfunction is linked to dysregulation of BDNF/TRKB, a pathway promoting neuroplasticity, neuronal survival and stress resilience.
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Multi-omics profiling of DNA methylation and gene expression alterations in human cocaine use disorder - Translational Psychiatry

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By Josef Frank, Naguib Mechawar, Gustavo Turecki, Judit Cabana-Domínguez, Bru Cormand, Janitza L. Montalvo-Ortiz, Anita C. Hansson, Marcella Rietschel, Rainer Spanagel, Stephanie Witt
| Nature Verified
Abstract Structural and functional changes of the brain are assumed to contribute to excessive cocaine intake, craving, and relapse in cocaine use disorder (CUD). Epigenetic and transcriptional changes were hypothesized as a molecular basis for CUD-associated brain alterations. Here we performed a multi-omics study of CUD by integrating epigenome-wide methylomic (N = 42) and transcriptomic (N = 25) data from the same individuals using postmortem brain tissue of Brodmann Area 9 (BA9).
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