Gender and age differences in the presentation of at-risk or probable Developmental Coordination Disorder in adults.

BACKGROUND: Developmental Coordination Disorder (DCD), also called Dyspraxia, is a common Neurodevelopmental Disorder (NDD) that affects motor coordination with a marked impact on both academic and day-to-day living activities. It is increasingly clear that NDDs such as Attention-Deficit/Hyperactivity Disorder and Autism Spectrum Disorder may present differently in males and females, resulting in underdiagnoses of women and girls. AIMS: To consider age and gender differences in the presentation of at-risk and probable DCD. METHODS AND PROCEDURES: A sample of 1,476 adults aged 16-60 years were surveyed online using the Adult DCD Checklist. OUTCOMES AND RESULTS: Women with at-risk (n = 1 8 6, 1 6. 6 %) or probable DCD (n = 6 4 3, 5 6. 6 %) reported significantly greater gross motor and non-motor difficulties and significantly greater impact on activities and participation, whereas men with at-risk (n = 58,16.3 %) or probable (n = 177,49.9 %), DCD reported significantly greater fine motor difficulties. Emerging adults (aged 16-25 years) with at-risk (n = 65,14.3 %) or probable (293,64.3 %) DCD reported significantly greater non-motor difficulty than adults (aged 26-60+ years) with at-risk (n = 179,17.5 %) or probable (n = 518, 50.8 %) DCD. CONCLUSIONS AND IMPLICATIONS: Both age and gender differences were found in the presentation of at-risk and probable DCD in adults. This may have implications for the development of future DCD assessment tools and for the training of front-line staff who may encounter individuals with DCD throughout their lives, including teachers, doctors and employers' Human Resources and Occupational Health staff.

Fetus-derived DLK1 is required for maternal metabolic adaptations to pregnancy and is associated with fetal growth restriction.

Pregnancy is a state of high metabolic demand. Fasting diverts metabolism to fatty acid oxidation, and the fasted response occurs much more rapidly in pregnant women than in non-pregnant women. The product of the imprinted DLK1 gene (delta-like homolog 1) is an endocrine signaling molecule that reaches a high concentration in the maternal circulation during late pregnancy. By using mouse models with deleted Dlk1, we show that the fetus is the source of maternal circulating DLK1. In the absence of fetally derived DLK1, the maternal fasting response is impaired. Furthermore, we found that maternal circulating DLK1 levels predict embryonic mass in mice and can differentiate healthy small-for-gestational-age (SGA) infants from pathologically small infants in a human cohort. Therefore, measurement of DLK1 concentration in maternal blood may be a valuable method for diagnosing human disorders associated with impaired DLK1 expression and to predict poor intrauterine growth and complications of pregnancy.

Phenotypic outcomes of imprinted gene models in mice: elucidation of pre- and postnatal functions of imprinted genes.

Genomic imprinting is an epigenetic process causing expression of a subset of genes in a parent-of-origin-specific manner. Among vertebrates, only therian mammals have been demonstrated to imprint, indicating that placentation and imprinting arose at similar time points in evolution and that imprinting may be involved in key mammal-specific processes. However, although several theories have been posited to explain the evolution of imprinting, each has shortcomings and none fully explains the wide variety of genes regulated by imprinting. In this review, we catalog the phenotypes associated with genetic mutation and overexpression at particular imprinted loci in order to consider the wide impact of imprinted genes on development. In addition to the well-described roles of imprinted genes in prenatal growth and placentation, more recent data emphasize that imprinted genes are critical for specific aspects of postnatal mammalian development involving adaptive processes, metabolism, and behavior.