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Lavinia Athanasiu

Researcher at University of Oslo

Publications -  63
Citations -  6027

Lavinia Athanasiu is an academic researcher from University of Oslo. The author has contributed to research in topics: Genome-wide association study & Schizophrenia. The author has an hindex of 24, co-authored 52 publications receiving 3536 citations. Previous affiliations of Lavinia Athanasiu include Oslo University Hospital.

Papers
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Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer's disease risk.

Iris E. Jansen, +65 more
- 01 Mar 2019 - 
TL;DR: A large genome-wide association study of clinically diagnosed AD and AD-by-proxy identifies new loci and functional pathways that contribute to AD risk and adds novel insights into the neurobiology of AD.
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Common genetic variants influence human subcortical brain structures.

Derrek P. Hibar, +344 more
- 09 Apr 2015 - 
TL;DR: In this paper, the authors conduct genome-wide association studies of the volumes of seven subcortical regions and the intracranial volume derived from magnetic resonance images of 30,717 individuals from 50 cohorts.
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Mapping genomic loci implicates genes and synaptic biology in schizophrenia

Vassily Trubetskoy, +432 more
- 08 Apr 2022 - 
TL;DR: In this article , a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals was conducted, and the authors reported common variant associations at 287 distinct genomic loci.
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New insights into the genetic etiology of Alzheimer’s disease and related dementias

Céline Bellenguez, +401 more
- 01 Apr 2022 - 
TL;DR: This paper performed a two-stage genome-wide association study with 111,326 clinically diagnosed/proxy AD cases and 677,663 controls and found 75 risk loci, of which 42 were new at the time of analysis.
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A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer's disease.

Douglas P Wightman, +89 more
- 01 Sep 2021 - 
TL;DR: This paper identified microglia, immune cells and protein catabolism as relevant genes for late-onset Alzheimer's disease, while identifying and prioritizing previously unidentified genes of potential interest.