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  • Neuroinformatics
  • National Institutes of Health

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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Hoogman, M.; van Rooij, D.; Klein, M.; Boedhoe, P.; +76 Authors

    Neuroimaging has been extensively used to study brain structure and function in individuals with attention deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) over the past decades. Two of the main shortcomings of the neuroimaging literature of these disorders are the small sample sizes employed and the heterogeneity of methods used. In 2013 and 2014, the ENIGMA-ADHD and ENIGMA-ASD working groups were respectively, founded with a common goal to address these limitations. Here, we provide a narrative review of the thus far completed and still ongoing projects of these working groups. Due to an implicitly hierarchical psychiatric diagnostic classification system, the fields of ADHD and ASD have developed largely in isolation, despite the considerable overlap in the occurrence of the disorders. The collaboration between the ENIGMA-ADHD and -ASD working groups seeks to bring the neuroimaging efforts of the two disorders closer together. The outcomes of case-control studies of subcortical and cortical structures showed that subcortical volumes are similarly affected in ASD and ADHD, albeit with small effect sizes. Cortical analyses identified unique differences in each disorder, but also considerable overlap between the two, specifically in cortical thickness. Ongoing work is examining alternative research questions, such as brain laterality, prediction of case-control status, and anatomical heterogeneity. In brief, great strides have been made toward fulfilling the aims of the ENIGMA collaborations, while new ideas and follow-up analyses continue that include more imaging modalities (diffusion MRI and resting-state functional MRI), collaborations with other large databases, and samples with dual diagnoses.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Serveur académique l...arrow_drop_down
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Serveur académique lausannois
    Review . 2022
    License: CC BY NC ND
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Serveur académique l...arrow_drop_down
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Serveur académique lausannois
      Review . 2022
      License: CC BY NC ND
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Maoxue Tang; Guangping Gao; Carlos B. Rueda; Hang Yu; +16 Authors

    Haploinsufficiency of the SLC2A1 gene and paucity of its translated product, the glucose transporter-1 (Glut1) protein, disrupt brain function and cause the neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS). There is little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatment for Glut1 DS. We used model mice to demonstrate that low Glut1 protein arrests cerebral angiogenesis, resulting in a profound diminution of the brain microvasculature without compromising the blood–brain barrier. Studies to define the temporal requirements for Glut1 reveal that pre-symptomatic, AAV9-mediated repletion of the protein averts brain microvasculature defects and prevents disease, whereas augmenting the protein late, during adulthood, is devoid of benefit. Still, treatment following symptom onset can be effective; Glut1 repletion in early-symptomatic mutants that have experienced sustained periods of low brain glucose nevertheless restores the cerebral microvasculature and ameliorates disease. Timely Glut1 repletion may thus constitute an effective treatment for Glut1 DS. Glut1-deficiency syndrome is a severe neurodevelopmental disorder characterized by low brain glucose and epileptic seizures. Tang et al. show that in model mice, low Glut1 leads to defects of the brain vasculature, and that AAV9-based gene therapy at pre- or early-symptomatic stages prevents the defects and mitigates disease.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Europe PubMed Centra...arrow_drop_down
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    Europe PubMed Central
    Article . 2017
    Data sources: PubMed Central
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Nature Communications
    Article
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    Data sources: UnpayWall
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    Nature Communications
    Article . 2017
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    Nature Communications
    Article . 2017 . Peer-reviewed
    License: CC BY
    Data sources: Crossref
    https://doi.org/10.7916/d89c76...
    Other literature type . 2017
    Data sources: Datacite
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Europe PubMed Centra...arrow_drop_down
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Europe PubMed Central
      Article . 2017
      Data sources: PubMed Central
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      Nature Communications
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      Nature Communications
      Article . 2017
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Nature Communications
      Article . 2017 . Peer-reviewed
      License: CC BY
      Data sources: Crossref
      https://doi.org/10.7916/d89c76...
      Other literature type . 2017
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Nandita Mukhopadhyay; Eleanor Feingold; Lina Moreno-Uribe; George L. Wehby; +17 Authors

    ABSTRACTOrofacial clefts (OFCs) are among the most common craniofacial birth defects and constitute a high public health burden around the world. OFCs are phenotypically heterogeneous, affecting only the lip, only the palate, or involving both the lip and palate. Cleft palate alone is demonstrably a genetically distinct abnormality from OFCs that involve the lip, therefore, it is common to study cleft lip (CL) in combination with cleft lip plus cleft palate (CLP) as a phenotypic group (i.e. cleft lip with or without cleft palate, CL/P), usually considering CLP to be a clinically more severe form of CL. However, even within CL/P, important genetic differences among subtypes may be present. The Pittsburgh Orofacial Cleft (Pitt-OFC) multiethnic study is a rich resource for the study of non-syndromic OFC, comprising a large number of families (∼12,000 individuals) from multiple populations worldwide: US and Europe (whites), Central and South America (mixed Native American, European and African), Asia, and Africa. In this study we focused on the CL/P families from this resource grouped into three non-overlapping family types: those with only CL affected members, only CLP affected members, or both CL and CLP. In all, seven total subtypes besides the combined CL/P phenotype, were defined based on the cleft type(s) that were present within pedigree members. The full sample for these analyses includes 2,218 CL and CLP cases along with 4,537 unaffected relatives, as well as 2,673 pure controls with no family history of OFC. Genome-wide association analyses were conducted within each subset, as well as the combined sample. Five novel genome-wide significant associations were observed: 3q29 (rs62284390, p=2.70E-08), 5p13.2 (rs609659, p= 4.57E-08), 7q22.1 (rs6465810, p= 1.25E-08), 19p13.3 (rs628271, p=1.90E-08) and 20q13.33 (rs2427238, p=1.51E-09). In addition, five significant and four suggestive associations confirmed regions previously published as OFC risk loci -PAX7, IRF6, FAM49A, DCAF4L2, 8q24.21,ARID3B, NTN1, TANC2and theWNT9B:WNT3gene cluster. At each of these loci, we compared effect sizes of associated SNPs observed across subtypes and the full sample, and found that certain loci were associated with a specific cleft type, and/or specific family types. Our findings indicate that risk factors differ between cleft and family types, but each cleft type also exhibits a certain degree of genetic heterogeneity.AUTHOR SUMMARYOrofacial clefts are common birth defects. Clefts often run in families, but their genetic basis is still an active area of investigation. In this study, we use an innovative approach to identify shared and unique genetic risk factors between two types of orofacial clefts - cleft lip and cleft lip plus cleft palate, by taking the patterns of different cleft types reported in families into account. Our study provides new insights into previously known genetic risk factors, but also identifies novel genetic regions that differentially impact the risk of developing cleft lip versus cleft lip plus cleft palate. This study contributes to the growing evidence that different sets of genes impact different forms of clefting and highlights the importance of incorporating information about familial affection patterns into analyses.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Genetic Epidemiologyarrow_drop_down
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    Genetic Epidemiology
    Article . Preprint . 2021
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Europe PubMed Central
    Other literature type . 2022
    Data sources: PubMed Central
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Genetic Epidemiology
    Article . 2022 . Peer-reviewed
    License: Wiley Online Library User Agreement
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    https://www.medrxiv.org/conten...
    Preprint
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    Data sources: UnpayWall
    image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Genetic Epidemiologyarrow_drop_down
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Genetic Epidemiology
      Article . Preprint . 2021
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Europe PubMed Central
      Other literature type . 2022
      Data sources: PubMed Central
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Genetic Epidemiology
      Article . 2022 . Peer-reviewed
      License: Wiley Online Library User Agreement
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      https://www.medrxiv.org/conten...
      Preprint
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      image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Tiril P. Gurholt; Tiril P. Gurholt; Tiril P. Gurholt; Unn K. Haukvik; +10 Authors

    AbstractSchizophrenia is a severe mental disorder with often a chronic course. Neuroimaging studies report brain abnormalities in both white and gray matter structures. However, the relationship between microstructural white matter differences and volumetric subcortical structures is not known.We investigated 30 long-term treated patients with schizophrenia (mean age 51.1±7.9 years, illness duration 27.6±8.0 years) and 42 healthy controls (mean age 54.1±9.1 years) using 3 T diffusion and structural magnetic resonance imaging. The free-water imaging method was used to model the diffusion signal, and subcortical volumes were obtained from FreeSurfer. We applied multiple linear regression to investigate associations between (i) patient status and regional white matter microstructure, (ii) medication dose or clinical symptoms on white matter microstructure in patients, and (iii) for interactions between subcortical volumes and diagnosis for microstructural white matter regions showing significant patient-control differences.The patients had significantly decreased free-water corrected fractional anisotropy (FAt), explained by decreased axial diffusivity and increased radial diffusivity (RDt) bilaterally in the anterior corona radiata (ACR) and the left anterior limb of the internal capsule (ALIC) compared to controls. In the fornix, the patients had significantly increased RDt. In patients, positive symptoms were associated with localized increased free-water and negative symptoms with localized decreased FAt and increased RDt. There were significant interactions between patient status and several subcortical structures on white matter microstructure and the free-water compartment for left ACR and fornix, and limited to the free-water compartment for right ACR and left ALIC. The Cohen’s d effect sizes were medium to large (0.61 to 1.20, absolute values).The results suggest a specific pattern of frontal white matter axonal degeneration and demyelination and fornix demyelination that is attenuated in the presence of larger structures of the limbic system in patients with chronic schizophrenia. Findings warrants replication in larger samples.

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    bioRxiv
    Preprint . 2019
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    Europe PubMed Central
    Article . 2020
    Data sources: PubMed Central
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    Frontiers in Psychiatry
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    https://www.duo.uio.no/bitstre...
    Preprint
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    Frontiers in Psychiatry
    Article . 2020 . Peer-reviewed
    License: CC BY
    Data sources: Crossref
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Frontiers in Psychiatry
    Article . 2020
    Data sources: DOAJ-Articles
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ bioRxivarrow_drop_down
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      bioRxiv
      Preprint . 2019
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      Europe PubMed Central
      Article . 2020
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      Frontiers in Psychiatry
      Article
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      Frontiers in Psychiatry
      Article . 2020 . Peer-reviewed
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      Frontiers in Psychiatry
      Article . 2020
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    Authors: Jenna C. Carlson; Nichole Nidey; Azeez Butali; Carmen Buxó Martinez; +15 Authors

    AbstractNonsyndromic cleft lip with or without cleft palate (NSCL/P) is the most common craniofacial birth defect in humans and is notable for its apparent sexual dimorphism where approximately twice as many males are affected as females. The sources of this disparity are largely unknown, but interactions between genetic and sex effects are likely contributors. We examined gene‐by‐sex (G × S) interactions in a worldwide sample of 2,142 NSCL/P cases and 1,700 controls recruited from 13 countries. First, we performed genome‐wide joint tests of the genetic (G) and G × S effects genome‐wide using logistic regression assuming an additive genetic model and adjusting for 18 principal components of ancestry. We further interrogated loci with suggestive results from the joint test ( p < 1.00 × 10 −5) by examining the G × S effects from the same model. Out of the 133 loci with suggestive results ( p < 1.00 × 10 −5) for the joint test, we observed one genome‐wide significant G × S effect in the 10q21 locus (rs72804706; p = 6.69 × 10 −9; OR = 2.62 CI [1.89, 3.62]) and 16 suggestive G × S effects. At the intergenic 10q21 locus, the risk of NSCL/P is estimated to increase with additional copies of the minor allele for females, but the opposite effect for males. Our observation that the impact of genetic variants on NSCL/P risk differs for males and females may further our understanding of the genetic architecture of NSCL/P and the sex differences underlying clefts and other birth defects.

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    bioRxiv
    Preprint . 2018
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    Genetic Epidemiology
    Article . 2018 . Peer-reviewed
    License: Wiley Online Library User Agreement
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    Europe PubMed Central
    Other literature type . 2018
    Data sources: PubMed Central
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      bioRxiv
      Preprint . 2018
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      Genetic Epidemiology
      Article . 2018 . Peer-reviewed
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      Europe PubMed Central
      Other literature type . 2018
      Data sources: PubMed Central
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      https://www.biorxiv.org/conten...
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    Authors: Sara A. Heyn; Ryan J. Herringa;

    Background Previous studies have identified structural brain abnormalities in pediatric PTSD. However, little is known about what structural brain substrates may confer recovery versus persistence of PTSD in the context of the developing brain. Methods This naturalistic longitudinal study used T1-weighted MRI to evaluate cortical thickness and surface area in youth with a PTSD diagnosis (n = 28) and typically developing healthy youth (TD; n = 27) at baseline and one-year follow-up. Of the PTSD group, 10 youth were remitters at one-year follow up while 18 had persistent PTSD. Whole-brain estimates of cortical thickness and surface area were extracted to identify differences in cortical architecture associated with PTSD remission and persistence as compared to typical development. Results Youth who achieved PTSD remission entered the study with significantly lower trauma exposure and reduced symptom severity as compared to nonremitters. PTSD persistence was associated with decreased surface area over time in the ventrolateral prefrontal cortex (vlPFC) as compared to both remitters and TD youth. In contrast, PTSD remission was associated with expansion of frontal pole surface area and ventromedial PFC (vmPFC) thickness over time. Across clinical groups, vmPFC thickness was further inversely associated with symptom severity. Conclusions To our knowledge, these findings represent the first report of cortical substrates underlying persistence versus remission in pediatric PTSD. Together, these findings suggest active structural developmental processes unique to both remission and nonremission in youth with PTSD. In particular, expansion of prefrontal regions implicated in emotion regulation may facilitate recovery from PTSD in youth and would warrant further study. Highlights • Neural correlates of clinical outcomes in pediatric PTSD are poorly understood. • Remission and persistence show unique patterns of cortical development over time. • Nonremitters exhibit atypical decreases in prefrontal, parietal, and occipital CSA. • PTSD remission was associated with cortical expansion in the prefrontal cortex.

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    Europe PubMed Central
    Article . 2019
    Data sources: PubMed Central
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    NeuroImage: Clinical
    Article . 2019
    Data sources: DOAJ-Articles
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    NeuroImage: Clinical
    Article . 2019 . Peer-reviewed
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      Europe PubMed Central
      Article . 2019
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      NeuroImage: Clinical
      Article . 2019
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      NeuroImage: Clinical
      Article . 2019 . Peer-reviewed
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    Authors: Matthias Kirschner; Golia Shafiei; Ross D. Markello; Carolina Makowski; +9 Authors

    Abstract Widespread structural brain abnormalities have been consistently reported in schizophrenia, but their relation to the heterogeneous clinical manifestations remains unknown. In particular, it is unclear whether anatomical abnormalities in discrete regions give rise to discrete symptoms or whether distributed abnormalities give rise to the broad clinical profile associated with schizophrenia. Here, we apply a multivariate data-driven approach to investigate covariance patterns between multiple-symptom domains and distributed brain abnormalities in schizophrenia. Structural magnetic resonance imaging and clinical data were derived from one discovery sample (133 patients and 113 controls) and one independent validation sample (108 patients and 69 controls). Disease-related voxel-wise brain abnormalities were estimated using deformation-based morphometry. Partial least-squares analysis was used to comprehensively map clinical, neuropsychological, and demographic data onto distributed deformation in a single multivariate model. The analysis identified 3 latent clinical-anatomical dimensions that collectively accounted for 55% of the covariance between clinical data and brain deformation. The first latent clinical-anatomical dimension was replicated in an independent sample, encompassing cognitive impairments, negative symptom severity, and brain abnormalities within the default mode and visual networks. This cognitive-negative dimension was associated with low socioeconomic status and was represented across multiple races. Altogether, we identified a continuous cognitive-negative dimension of schizophrenia, centered on 2 intrinsic networks. By simultaneously taking into account both clinical manifestations and neuroanatomical abnormalities, the present results open new avenues for multi-omic stratification and biotyping of individuals with schizophrenia.

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    medRxiv
    Preprint . 2020
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    Europe PubMed Central
    Article . 2020
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    Schizophrenia Bulletin
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    Schizophrenia Bulletin
    Article . 2020 . Peer-reviewed
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      Preprint . 2020
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      Article . 2020
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      Schizophrenia Bulletin
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      Schizophrenia Bulletin
      Article . 2020 . Peer-reviewed
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    Authors: Martine Hoogman; Daan van Rooij; Marieke Klein; Premika S.W. Boedhoe; +76 Authors

    Human brain mapping 43(1), 37-55 (2022). doi:10.1002/hbm.25029 special issue: "Special Issue: The ENIGMA Consortium: the first 10 years / Issue Edited by: P.M. Thompson, N. Jahanshad, L. Schmaal, J.A. Turner, A. Winkler, S.I. Thomopoulos, G.F. Egan, P. Kochunov" Published by Wiley-Liss, New York, NY

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    Europe PubMed Central
    Article . 2020
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    NARCIS
    Article . 2022
    Data sources: NARCIS
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    ZENODO
    Article . 2020
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    ZENODO
    Article . 2020
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    Human Brain Mapping
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      Human Brain Mapping
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Hoogman, M.; van Rooij, D.; Klein, M.; Boedhoe, P.; +76 Authors

    Neuroimaging has been extensively used to study brain structure and function in individuals with attention deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) over the past decades. Two of the main shortcomings of the neuroimaging literature of these disorders are the small sample sizes employed and the heterogeneity of methods used. In 2013 and 2014, the ENIGMA-ADHD and ENIGMA-ASD working groups were respectively, founded with a common goal to address these limitations. Here, we provide a narrative review of the thus far completed and still ongoing projects of these working groups. Due to an implicitly hierarchical psychiatric diagnostic classification system, the fields of ADHD and ASD have developed largely in isolation, despite the considerable overlap in the occurrence of the disorders. The collaboration between the ENIGMA-ADHD and -ASD working groups seeks to bring the neuroimaging efforts of the two disorders closer together. The outcomes of case-control studies of subcortical and cortical structures showed that subcortical volumes are similarly affected in ASD and ADHD, albeit with small effect sizes. Cortical analyses identified unique differences in each disorder, but also considerable overlap between the two, specifically in cortical thickness. Ongoing work is examining alternative research questions, such as brain laterality, prediction of case-control status, and anatomical heterogeneity. In brief, great strides have been made toward fulfilling the aims of the ENIGMA collaborations, while new ideas and follow-up analyses continue that include more imaging modalities (diffusion MRI and resting-state functional MRI), collaborations with other large databases, and samples with dual diagnoses.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Serveur académique l...arrow_drop_down
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Serveur académique lausannois
    Review . 2022
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Serveur académique l...arrow_drop_down
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Serveur académique lausannois
      Review . 2022
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Maoxue Tang; Guangping Gao; Carlos B. Rueda; Hang Yu; +16 Authors

    Haploinsufficiency of the SLC2A1 gene and paucity of its translated product, the glucose transporter-1 (Glut1) protein, disrupt brain function and cause the neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS). There is little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatment for Glut1 DS. We used model mice to demonstrate that low Glut1 protein arrests cerebral angiogenesis, resulting in a profound diminution of the brain microvasculature without compromising the blood–brain barrier. Studies to define the temporal requirements for Glut1 reveal that pre-symptomatic, AAV9-mediated repletion of the protein averts brain microvasculature defects and prevents disease, whereas augmenting the protein late, during adulthood, is devoid of benefit. Still, treatment following symptom onset can be effective; Glut1 repletion in early-symptomatic mutants that have experienced sustained periods of low brain glucose nevertheless restores the cerebral microvasculature and ameliorates disease. Timely Glut1 repletion may thus constitute an effective treatment for Glut1 DS. Glut1-deficiency syndrome is a severe neurodevelopmental disorder characterized by low brain glucose and epileptic seizures. Tang et al. show that in model mice, low Glut1 leads to defects of the brain vasculature, and that AAV9-based gene therapy at pre- or early-symptomatic stages prevents the defects and mitigates disease.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Europe PubMed Centra...arrow_drop_down
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    Europe PubMed Central
    Article . 2017
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    Nature Communications
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    Nature Communications
    Article . 2017
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    Nature Communications
    Article . 2017 . Peer-reviewed
    License: CC BY
    Data sources: Crossref
    https://doi.org/10.7916/d89c76...
    Other literature type . 2017
    Data sources: Datacite
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