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Showing 1–18 of 18 results
Advanced filters: Author: Johan Schwab Clear advanced filters
  • Genomic analyses applied to 14 childhood- and adult-onset psychiatric disorders identifies five underlying genomic factors that explain the majority of the genetic variance of the individual disorders.

    • Andrew D. Grotzinger
    • Josefin Werme
    • Jordan W. Smoller
    ResearchOpen Access
    Nature
    Volume: 649, P: 406-415
  • There is currently no disease-modifying treatment for Parkinson’s disease, a common neurodegenerative disorder. Here, the authors use genetic variation associated with gene and protein expression to find putative drug targets for Parkinson’s disease using Mendelian randomization of the druggable genome.

    • Catherine S. Storm
    • Demis A. Kia
    • Nicholas W. Wood
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-14
  • A genome-wide association study including over 76,000 individuals with schizophrenia and over 243,000 control individuals identifies common variant associations at 287 genomic loci, and further fine-mapping analyses highlight the importance of genes involved in synaptic processes.

    • Vassily Trubetskoy
    • Antonio F. Pardiñas
    • Jim van Os
    Research
    Nature
    Volume: 604, P: 502-508
  • Phytoplankton account for a large proportion of global primary production and comprise a number of phylogenetically distinct lineages. Here, Uwizeye et al. use FIB-SEM to study ultrastructural plasticity of 7 distinct taxa and describe how subcellular organisation is linked to energy metabolism.

    • Clarisse Uwizeye
    • Johan Decelle
    • Giovanni Finazzi
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-12
  • Lebedeva et al. show that unlike Bilateria, the embryo of the cnidarian Nematostella specifies its endomesoderm in the β-catenin-negative domain. In contrast, subsequent β-catenin-dependent axial patterning acts similarly in Cnidaria and Bilateria.

    • Tatiana Lebedeva
    • Johan Boström
    • Grigory Genikhovich
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-10
  • Schwab et al. evaluate patients with chronic urticaria (CU) in relation to COVID-19 infection and mRNA vaccination. CU post-vaccination was not directly associated with COVID infection nor atopy and initiates independent of vaccine sensitization.

    • Johan Schwab
    • Mathilde Foglierini
    • Yannick D. Muller
    ResearchOpen Access
    Communications Medicine
    Volume: 4, P: 1-10
  • Stratified medicine promises to tailor treatment for individual patients, however it remains a major challenge to leverage genetic risk data to aid patient stratification. Here the authors introduce an approach to stratify individuals based on the aggregated impact of their genetic risk factor profiles on tissue-specific gene expression levels, and highlight its ability to identify biologically meaningful and clinically actionable patient subgroups, supporting the notion of different patient ‘biotypes’ characterized by partially distinct disease mechanisms.

    • Lucia Trastulla
    • Georgii Dolgalev
    • Michael J. Ziller
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-28
  • The CNV analysis group of the Psychiatric Genomic Consortium analyzes a large schizophrenia cohort to examine genomic copy number variants (CNVs) and disease risk. They find an enrichment of CNV burden in cases versus controls and identify 8 genome-wide significant loci as well as novel suggestive loci conferring either risk or protection to schizophrenia.

    • Christian R Marshall
    • Daniel P Howrigan
    • Jonathan Sebat
    Research
    Nature Genetics
    Volume: 49, P: 27-35
  • Sexual dimorphism in genetic vulnerability to schizophrenia, systemic lupus erythematosus and Sjögren’s syndrome is linked to differential protein abundance from alleles of complement component 4.

    • Nolan Kamitaki
    • Aswin Sekar
    • Steven A. McCarroll
    Research
    Nature
    Volume: 582, P: 577-581
  • Relatives of patients with amyotrophic lateral sclerosis have an unexpectedly high incidence of schizophrenia. Here, the authors show a genetic link between the two conditions, suggesting shared neurobiological mechanisms.

    • Russell L. McLaughlin
    • Dick Schijven
    • Michael C. O’Donovan
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-12
  • The authors defined a roadmap for investigating the genetic covariance between structural or functional brain phenotypes and risk for psychiatric disorders. Their proof-of-concept study using the largest available common variant data sets for schizophrenia and volumes of several (mainly subcortical) brain structures did not find evidence of genetic overlap.

    • Barbara Franke
    • Jason L Stein
    • Patrick F Sullivan
    Research
    Nature Neuroscience
    Volume: 19, P: 420-431
  • Schizophrenia is a highly heritable genetic disorder, however, identification of specific genetic risk variants has proven difficult because of its complex polygenic nature—a large multi-stage genome-wide association study identifies 128 independent associations in over 100 loci (83 of which are new); key findings include identification of genes involved in glutamergic neurotransmission and support for a link between the immune system and schizophrenia.

    • Stephan Ripke
    • Benjamin M. Neale
    • Michael C. O’Donovan
    Research
    Nature
    Volume: 511, P: 421-427
  • The Schizophrenia Psychiatric Genome-Wide Association Study Consortium reports five genetic loci newly associated with risk of schizophrenia, involving 17,836 cases of schizophrenia and 33,859 healthy controls. The new locus with the strongest support of association was located within an intron for microRNA 137, a known regulator of neuronal development. Four other genome-wide significant loci for schizophrenia contain predicted targets of MIR137, suggesting that disruption to pathways involving MIR137 may be an etiologic mechanism in schizophrenia.

    • Stephan Ripke
    • Alan R Sanders
    • Pablo V Gejman
    Research
    Nature Genetics
    Volume: 43, P: 969-976