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We examined more than 38,000 spouse pairs from four neurodevelopmental disease cohorts and the UK Biobank to identify phenotypic and genetic patterns in parents associated with neurodevelopmental disease risk in children. We identified correlations between six phenotypes in parents and children, including correlations of clinical diagnoses such as obsessive-compulsive disorder (R=0.31-0.49, p<0.001), and two measures of sub-clinical autism features in parents affecting several autism severity measures in children, such as bi-parental mean Social Responsiveness Scale (SRS) scores affecting proband SRS scores (regression coefficient=0.11, p=0.003). We further describe patterns of phenotypic and genetic similarity between spouses, where spouses show both within- and cross-disorder correlations for seven neurological and psychiatric phenotypes, including a within-disorder correlation for depression (R=0.25-0.72, p<0.001) and a cross-disorder correlation between schizophrenia and personality disorder (R=0.20-0.57, p<0.001). Further, these spouses with similar phenotypes were significantly correlated for rare variant burden (R=0.07-0.57, p<0.0001). We propose that assortative mating on these features may drive the increases in genetic risk over generations and the appearance of "genetic anticipation" associated with many variably expressive variants. We further identified parental relatedness as a risk factor for neurodevelopmental disorders through its inverse correlations with burden and pathogenicity of rare variants and propose that parental relatedness drives disease risk by increasing genome-wide homozygosity in children (R=0.09-0.30, p<0.001). Our results highlight the utility of assessing parent phenotypes and genotypes in predicting features in children carrying variably expressive variants and counseling families carrying these variants.
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http://dx.doi.org/10.1101/2023.05.18.23290169 | DOI Listing |
Curr Opin Virol
September 2025
Infection Biology, Global Center for Pathogen and Human Health Research, Cleveland Clinic, Cleveland, OH 44195, USA; Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH 44195, USA. Electronic address:
Intracranial calcifications (ICCs) are a characteristic neuropathological feature of several congenital viral infections, including Zika virus (ZIKV), cytomegalovirus (CMV), and lymphocytic choriomeningitis virus (LCMV). These lesions are linked to severe neurodevelopmental outcomes, such as microcephaly, epilepsy, and cognitive deficits, yet the mechanisms underlying their formation and resolution remain unclear. ICCs are thought to arise from an imbalance in osteogenic and osteolytic signaling in the developing brain.
View Article and Find Full Text PDFMol Psychiatry
September 2025
Department of Child and Adolescent Psychiatry and Psychology, Erasmus MC University Medical Center Rotterdam, Rotterdam, the Netherlands.
Epigenetic processes, such as DNA methylation, show potential as biological markers and mechanisms underlying gene-environment interplay in the prediction of mental health and other brain-based phenotypes. However, little is known about how peripheral epigenetic patterns relate to individual differences in the brain itself. An increasingly popular approach to address this is by combining epigenetic and neuroimaging data; yet, research in this area is almost entirely comprised of cross-sectional studies in adults.
View Article and Find Full Text PDFJ Biol Chem
September 2025
Department of Integrative Structural and Computational Biology, The Scripps Research Institute, La Jolla, California, USA.
Aminoacyl-tRNA synthetases (aaRSs) catalyze the aminoacylation of tRNA with their cognate amino acids, an essential step in protein biosynthesis. While biallelic mutations in aaRSs often result in severe multi-organ dysfunction accompanied by developmental delays, monoallelic mutations typically cause milder, tissue-specific symptoms. However, a de novo monoallelic nonsense mutation (R534*) in the asparaginyl-tRNA synthetase (AsnRS)-resulting in a premature stop codon and 15-residue C-terminal truncation-has been identified in multiple families and is associated with severe neurodevelopmental symptoms.
View Article and Find Full Text PDFCell Rep
September 2025
Virginia Tech Fralin Biomedical Research Institute Cancer Research Center DC, Children's National Research & Innovation Campus, Washington, DC, USA; Department of Biomedical Sciences and Pathobiology (DBSP), Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA, USA; Center
Nuclear receptor binding set domain protein 1 (NSD1) is a key histone methyltransferase that catalyzes di-methylation of lysine 36 of histone H3 (H3K36me2), essential for active chromatin domains. While the loss of NSD1 activity halts embryonic development and its aberrant gain drives oncogenesis in leukemia and glioma, the regulatory mechanisms remain poorly understood. Here, we uncover that NSD1 requires allosteric activation through the aromatic pocket of its Pro-Trp-Trp-Pro 2 (PWWP2) domain.
View Article and Find Full Text PDFMol Genet Genomics
September 2025
Human Phenome Institute, MOE Key Laboratory of Contemporary Anthropology, Zhangjiang Fudan International Innovation Center, Fudan University, 825 Zhangheng Road, Shanghai, 201203, China.
Accurate variant calling is essential for next-generation sequencing (NGS)-based diagnosis of rare diseases, yet most benchmarking studies have focused on standard cell lines or trio-based samples, with limited relevance to sporadic cases. Here, we systematically compared the performance of DeepVariant and GATK HaplotypeCaller in two Chinese cohorts of patients with sporadic epilepsy (EP) and autism spectrum disorder (ASD). DeepVariant exhibited higher precision and sensitivity in detecting single nucleotide variants (SNVs), while GATK showed a distinct advantage in identifying rare variants, which are often key to understanding the genetic basis of rare diseases.
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