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Hans J. Grabe

Researcher at Greifswald University Hospital

Publications -  29
Citations -  2607

Hans J. Grabe is an academic researcher from Greifswald University Hospital. The author has contributed to research in topics: Major depressive disorder & Genome-wide association study. The author has an hindex of 18, co-authored 29 publications receiving 1597 citations. Previous affiliations of Hans J. Grabe include University of Greifswald & University of Southern California.

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The genetic architecture of the human cerebral cortex

Katrina L. Grasby, +359 more
- 20 Mar 2020 - 
TL;DR: Results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness and find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function.
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ENIGMA and global neuroscience: A decade of large-scale studies of the brain in health and disease across more than 40 countries

Paul M. Thompson, +213 more
TL;DR: This review summarizes the last decade of work by the ENIGMA Consortium, a global alliance of over 1400 scientists across 43 countries, studying the human brain in health and disease, and highlights the advantages of collaborative large-scale coordinated data analyses for testing reproducibility and robustness of findings.
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Novel genetic loci underlying human intracranial volume identified through genome-wide association

Hieab H.H. Adams, +435 more
- 01 Dec 2016 - 
TL;DR: Variants for intracranial volume were also related to childhood and adult cognitive function, and Parkinson's disease, and were enriched near genes involved in growth pathways, including PI3K-AKT signaling.
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Minimal phenotyping yields genome-wide association signals of low specificity for major depression

TL;DR: In this paper, the authors report differences in genetic architecture between depression defined by minimal phenotyping and strictly defined major depressive disorder (MDD): the former has a lower genotype-derived heritability that cannot be explained by inclusion of milder cases and a higher proportion of the genome contributing to this shared genetic liability with other conditions than for strictly defined MDD.