Doctor Evelyn Andersson Hagen!

Congrats Evelyn! She is the 4th PhD student to graduate from our lab and she defended her thesis very well the past Friday. Big thank you to everyone involved!

 

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Evelyn in defense mode.

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From left: Co-supervisor Erik Hedman-Lagerlöf, examination board member Lisa Thorell, main supervisor Christian Rück, Evelyn, co-supervisor Martin Schalling and Cattis Lavebratt, opponent Jönsson, examination board member Lars Westberg and session chair Viktor Kaldo.

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Party!

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Winning shoes!

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Opponent Erik Jönsson, Oslo University.

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ICBT FTW!

GDPR

Från och med idag ersätter Dataskyddsförordningen GDPR den tidigare Personuppgiftslagen (PUL). Detta gäller alla våra studier.

Evelyn nailed it!

Evelyn Andersson Hagen today nailed her thesis at the KI Library. This is symbol of her thesis now being out in the public. She will defend her thesis June 1st. Everyone is welcome! Details here.

Big thanks to all the participants of the studies, the involved clinicians of Internetpsykiatrienheten and to the co-supervisors Nils Lindefors, Martin Schalling, Catharina Lavebratt and Erik Hedman-Lagerlöf.

The thesis is here (pdf).

 

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‘Game-Changing’ Depression Study Discovers 44 Genes

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We are proud that a landmark study of depression genetics published in Nature Genetics has Professor Manuel Mattheisen as one of the lead authors. Manuel is a Professor at Würzburg University but also affiliated to our group at Karolinska Institutet.

The authors conducted a genome-wide association meta-analysis based in 135,458 cases and 344,901 controls and identified 44 independent and significant loci. The genetic findings were associated with clinical features of major depression and implicated brain regions exhibiting anatomical differences in cases. Targets of antidepressant medications and genes involved in gene splicing were enriched for smaller association signal. We found important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia: lower educational attainment and higher body mass were putatively causal, whereas major depression and schizophrenia reflected a partly shared biological etiology. All humans carry lesser or greater numbers of genetic risk factors for major depression. These findings help refine the basis of major depression and imply that a continuous measure of risk underlies the clinical phenotype.

Here is a commentary in The Guardian.

Nature Genetics volume 50pages 668–681 (2018)

Full paper: https://www.nature.com/articles/s41588-018-0090-3

JOBB: Vi söker projektledare, forskningsassistent och forskningssjuksköterska

Vi söker tre medarbetare för att arbeta med oss med att lösa vad orsakerna till sjukdomar som OCD är.

 

Forskningssjuksköterska:

https://ki.mynetworkglobal.com/se/what:job/jobID:191723/type:job/where:4/apply:1

Forskningsassistent:

https://ki.mynetworkglobal.com/se/what:job/jobID:192808/type:job/where:4/apply:1

Projektsamordnare:

https://ki.mynetworkglobal.com/se/what:job/jobID:192810/type:job/where:4/apply:1

 

New study finds 4 OCD related genes

A new study just out in Nature Communications:

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Obsessive-compulsive disorder is a severe psychiatric disorder linked to abnormalities in glutamate signaling and the cortico-striatal circuit. We sequenced coding and regulatory elements for 608 genes potentially involved in obsessive-compulsive disorder in human, dog, and mouse. Using a new method that prioritizes likely functional variants, we compared 592 cases to 560 controls and found four strongly associated genes, validated in a larger cohort. NRXN1 and HTR2A are enriched for coding variants altering postsynaptic protein-binding domains. CTTNBP2 (synapse maintenance) and REEP3 (vesicle trafficking) are enriched for regulatory variants, of which at least six (35%) alter transcription factor-DNA binding in neuroblastoma cells. NRXN1 achieves genome-wide significance (p = 6.37 × 10−11) when we include 33,370 population-matched controls. Our findings suggest synaptic adhesion as a key component in compulsive behaviors, and show that targeted sequencing plus functional annotation can identify potentially causative variants, even when genomic data are limited.

New Scientist reported about the study and there is a short video here: