Author

Friederike Sophie David

University of BonnORCID 0000-0001-9521-5669Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Genetic & Genomic Medicine· 2 Neuroscience· 1

Signature Assays, Organisms & Methods

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Research Focus:GWAS / association mapping· 2 Assay:GWAS summary statistics· 2 Organism:human· 2 Approach:statistical model· 2 Assay:clinical cohort / trial· 1 Research Focus:drug response / drug discovery· 1 Research Focus:eQTL / molecular QTL mapping· 1 Approach:experimental assay· 1

Frequent Co-Authors

Alfredo B. Cuellar BarbozaiD· 2 shared Anastasia AntoniouiD· 2 shared Anders Martin DaleiD· 2 shared Ben Michael BrumptoniD· 2 shared Brandon J. CoombesiD· 2 shared Cristiana CruceanuiD· 2 shared Dennis Hellgren· 2 shared Diego AlbaniiD· 2 shared

Activity by Year

2021-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersGenetic & Genomic Medicine

Alfredo B. Cuellar BarbozaORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

Genetic & Genomic MedicinemedRxivPreprintJun 23, 2025

Genomic dimensions deconstruct the clinical heterogeneity of bipolar disorder

Tracey van der Veen, Markos Tesfaye, Jessica Mei Kay Yang…·Melvin G. McInnis

This study identifies genetic risk loci and factors underlying clinical subtypes of bipolar disorder using GWAS and meta-analysis.

1 citation

humanGWAS summary statistics

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Genetic & Genomic MedicineNature GeneticsPeer-reviewedMay 17, 2021

✦ In-depth digest

Genome-wide association study of over 40,000 bipolar disorder cases provides new insights into the underlying biology

Niamh Mullins, Andreas J. Forstner, Kevin Sean O’Connell…·Janos L. Kalman

Meta-analysis of 41,917 European-ancestry bipolar disorder cases versus 371,549 controls yields 64 risk loci (33 novel), neuronal and synaptic gene enrichment, and 15 eQTL-prioritized genes.

1,517 citationstop 1%

humanGWAS summary statistics

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NeuroscienceProceedings of the National Academy of SciencesPeer-reviewedJan 5, 2021

A CRISPR-Cas9-engineered mouse model for GPI-anchor deficiency mirrors human phenotypes and exhibits hippocampal synaptic dysfunctions

Miguel Rodríguez de los Santos, Marion Rivalan, Friederike Sophie David…·Peter Michael Krawitz

This paper introduces a CRISPR-Cas9-engineered mouse model for GPI-anchor deficiency that mirrors human phenotypes, including cognitive impairments and epilepsy, and identifies synaptic transmission deficits.

15 citations

mouseexperimental assay

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