Mikael Landén

Ultra-rare damaging coding variants in 87,959 schizophrenia cases and 150,587 controls implicate 40 genes (16 exome-wide, 24 at 5% FDR), half overlapping autism, developmental delay or bipolar genes.

This study identifies BHLHE41 as a key regulator of lithium response in bipolar disorder by showing its role in neuronal excitability and synaptic plasticity through genetic and cellular analyses.

This paper conducts a GWAS of distressing premenstrual symptoms (DPS) in two Nordic populations, identifying a SNP associated with DPS and genetic correlations to psychiatric disorders.

The paper introduces a scalable toolkit for 3D surface-based brain analysis, demonstrating its utility in mapping subcortical shape variations across 21 international samples.

The paper assesses neuronal and non-neuronal cell turnover in the hippocampus of individuals with alcohol or cocaine abuse compared to healthy controls, finding no significant difference in turnover rates between groups.

The paper identifies genetic regulators of 184 neuro-related proteins in human plasma and links them to disease traits and drug targets.

This study conducts a large-scale GWAS of OCD, identifying 15 new genome-wide significant loci and linking OCD to multiple cortical regions and cell types.

The paper identifies pQTLs for 91 plasma proteins, finds novel associations, and uses MR to uncover causal roles in immune-mediated diseases, suggesting new therapeutic targets.

This study examines the genetic and clinical associations of adult weight trajectories using EHR data, identifying disease links and genetic risk factors for weight patterns.

This study uses transcriptomic imputation to translate AN GWAS findings into gene expression associations, revealing 47 genes linked to AN and their clinical consequences in a biobank cohort.

The paper reports exome sequencing findings in bipolar disorder, identifying AKAP11 as a shared risk gene with schizophrenia through ultra-rare protein-truncating variants.

The paper identifies pQTLs for cardiovascular proteins and uses them to evaluate drug targets and suggest new candidates for precision medicine.

The study finds that rare copy number variants (CNVs) contribute to bipolar disorder risk primarily in schizoaffective disorder bipolar type cases, with differences in CNV burden and schizophrenia polygenic risk scores between subtypes.

The paper shows that polygenic scores for depression traits predict lithium response in bipolar disorder patients, with lower genetic load linked to better treatment outcomes.

The paper describes the methods and recruitment strategies of the Anorexia Nervosa Genetics Initiative (ANGI), which successfully enrolled 13,364 individuals with AN and controls for genetic research.

This paper validates EHR-based BD phenotyping algorithms by showing their genetic correlation with traditional BD cases, suggesting they identify genetically similar cases.

This paper uses transcriptomic imputation to identify gene-tissue associations linked to Anorexia Nervosa risk, finding significant links in both brain and metabolic tissues.

This study finds that a higher genetic risk for schizophrenia is linked to poorer lithium response in bipolar disorder patients, suggesting potential for personalized treatment strategies.