Peter Holmans

The paper shows rare genetic variants influence participation in cognitive tests of the UK Biobank, affecting the representativeness of the cohort and power of association studies.

The paper introduces an adversarial neural network to identify genetic resilience markers in Alzheimer's disease, finding five SNPs associated with resilience independent of polygenic risk scores.

This study identifies genetic variants differentially associated with schizophrenia and bipolar disorder using CC-GWAS, finding 19 loci with divergent effects and biological themes related to neuronal function.

This study uses human iPSC-derived microglia with high polygenic AD risk to identify functional impairments in immune response, mitochondrial function, and amyloid-beta uptake.

The paper investigates the effect of rare coding variants in schizophrenia-associated genes on generalised cognition in the UK Biobank using exome-sequencing data.

The paper examines the expression patterns of dystonia-causing genes across developmental stages and brain regions to identify key areas and cell types for disease modeling and therapy.

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

The paper investigates the association between neurodevelopmental copy number variants (ND-CNVs) and increased risk of internalising and cardiometabolic multimorbidity using UK Biobank data.

This paper investigates how genetic liabilities shared and differentiating between schizophrenia and bipolar disorder relate to cognition and educational attainment using UK Biobank data.

This study identifies rare coding variants in STAG1 and ZNF136 associated with schizophrenia using exome sequencing data from 28,898 cases and 103,041 controls.

This study examines irritability in young people with neurodevelopmental copy number variants (ND-CNVs) and finds it is more common than in controls, independent of psychiatric diagnoses or IQ.

The paper identifies genetic modifiers of somatic CAG expansion and clinical phenotypes in Huntington's disease, revealing shared and tissue-specific effects on disease timing and pathogenic processes.

This study identifies somatic copy number variants (sCNVs) in schizophrenia cases, revealing their contribution to risk and specific NRXN1 disruptions.

The paper uses brain cell-type-specific protein interactomes to interpret genetic data in schizophrenia and identifies enriched networks and genes associated with the disease.

This study examines how genetic risk for Alzheimer's disease affects structural brain networks in young adults using MRI and genotype data.

The paper identifies a tandem hexamer repeat in TCERG1 that modifies age at motor onset in Huntington's disease, explaining the effect of a previously associated SNP.

This study identifies genetic resilience factors for Alzheimer's disease by constructing polygenic resilience scores that reduce genetic risk penetrance and correlate with polygenic risk scores in unaffected individuals.

The paper analyzes Alzheimer's disease polygenic risk scores using RNA-sequencing to identify novel biological pathways and common mechanisms between case/control classification and PRS associations.

The paper identifies FAN1 nuclease activity as a modifier of CAG expansion and age at onset in Huntington's disease through exome sequencing and functional validation.

This study identifies sex-dependent genetic risk loci shared and specific to mood and psychotic disorders using genome-wide interaction analysis.

The paper identifies shared disruptive coding mutations between schizophrenia, autism spectrum disorders, and other developmental disorders, suggesting overlapping molecular aetiology.

This study shows that altering Spi1 levels in mouse microglia affects transcriptomic pathways, suggesting a link between Spi1 and AD-related immune responses.

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.

The paper compares ten polygenic score methods for psychiatric disorders across multiple cohorts, finding that some methods significantly improve prediction statistics over the baseline PC+T method.

The paper identifies human-lineage-specific genomic elements, called CNCRs, and shows their enrichment in neurological disease genes and APOE intron-3 retention transcripts in Alzheimer's disease.

This study examines the prevalence, timing, and functional impact of psychiatric, cognitive, and motor symptoms in Huntington's disease gene carriers using clinical data from a large cohort.

The paper examines the developmental expression of genes related to voltage-gated cation channels and their association with psychiatric disorders, finding that gene expression patterns vary with age and disorder type.

The paper examines the genetic association of FMRP targets with schizophrenia, major depressive disorder, and bipolar disorder, finding enrichment for risk alleles and variants in these disorders.

This study identifies cell-type-specific expression of dystonia-associated genes and links them to shared genetic and biological mechanisms with psychiatric disorders.