Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder characterized by impaired social communication and restricted and repetitive behaviors (RRBs). Over the past decade, neuroimaging studies have provided considerable insights underlying neurobiological mechanisms of ASD. In this review, we introduce recent findings from brain imaging studies to characterize the brains of ASD across the human lifespan. Results of structural Magnetic Resonance Imaging (MRI) studies dealing with total brain volume, regional brain structure and cortical area are summarized. Using task-based functional MRI (fMRI), many studies have shown dysfunctional activation in critical areas of social communication and RRBs. We also describe several data to show abnormal connectivity in the ASD brains. Finally, we suggest the possible strategies to study ASD brains in the future.

PurposeWe aimed to determine whether Autism Spectrum Disorder (ASD) would show neural abnormality of the social reward system using functional MRI (fMRI).Materials and Methods27 ASDs and 12 typically developing controls (TDCs) participated in this study. The social reward task was developed, and all participants performed the task during fMRI scanning.ResultsASDs and TDCs with a social reward learning effect were selected on the basis of behavior data. We found significant differences in brain activation between the ASDs and TDCs showing a social reward learning effect. Compared with the TDCs, the ASDs showed reduced activity in the right dorsolateral prefrontal cortex, right orbitofrontal cortex, right parietal lobe, and occipital lobe; however, they showed increased activity in the right parahippocampal gyrus and superior temporal gyrus.ConclusionThese findings suggest that there might be neural abnormality of the social reward learning system of ASDs. Although this study has several potential limitations, it presents novel findings in the different neural mechanisms of social reward learning in children with ASD and a possible useful biomarker of high-functioning ASDs.

Background The association between dyslipidemia and atopic dermatitis in children is unclear. This study investigated the association between dyslipidemia and atopic dermatitis in children by analysis of disease onset, risk factors, and disease severity. Methods Subset I examined 7‐year‐old children in elementary school (n = 248), and Subset II was a retrospective long‐term follow‐up hospital‐based study (n = 52 725) conducted from 1986 to 2016 that used propensity score matching. In the Subset I study, total cholesterol (TC), high‐density lipoprotein cholesterol (HDL‐C), low‐density lipoprotein cholesterol (LDL‐C), and triglycerides (TG) were determined, and the SCORing Atopic Dermatitis (SCORAD) index was determined. In the Subset II study, the time of atopic dermatitis onset was determined for asymptomatic subjects whose TC levels were below or above 170 mg/dL. Results Our Subset I study indicated that children with atopic dermatitis (n = 69, 27.8%) had significantly higher levels of TC and TG, and that the SCORAD index had significant associations with high levels of TC and TG, and a low level of HDL‐C. Our Subset II study (1722 with high TC and 6735 with normal TC after propensity score matching) indicated the high TC group had a greater hazard ratio (HR) for the onset of atopic dermatitis (consensus‐based HR: 2.47; 95% CI: 1.23, 5.06, P = .012) during 5 years. Conclusion An abnormal blood lipid profile in children is associated with the presence of atopic dermatitis and the SCORAD index. The risk of atopic dermatitis onset was significantly greater with high levels of TC.

Background: Smell dysfunction is highly prevalent worldwide and has adverse effects on quality of life. Smell loss in rhinitis subjects is mainly caused by mechanical obstruction of odorant transmission due to mucosal type 2 inflammation. We determined the association of 25-hydroxyvitamin D (25[OH]D) levels with the severity of smell dysfunction in children. Methods: We measured the olfactory threshold score in a total of 518 children (10-12 years old, 264 boys) using the Sniffin' Sticks kit, and the children were divided into tertiles according to olfactory threshold score. We also assessed serum 25[OH] D level, common aeroallergen-specific immunoglobulin E, rhinitis severity with visual analog scale, and the Total Four Symptom Score, and pre-and post-decongestant nasal patency with acoustic rhinometry. Results: The children with 25(OH)D deficiency had significantly reduced mean olfactory threshold scores when compared to those with 25(OH)D levels of ≥20.0 ng/ mL (6.56 ± 3.54 and 7.28 ± 3.87, respectively, P = .036). The proportion of loss of smell function and pre-decongestant nasal patency significantly associated with low 25(OH)D levels (chi-square trend test, P for trend = .007). Likewise, after adjustment for confounders, children with smell loss (third tertile) were significantly associated with low 25(OH)D level (aβ=−0.062, 95% CI=−0.064 to −0.060, P = .009) independent of aeroallergen sensitization, and a low pre-decongestant nasal patency. Conclusions: 25-Hydroxyvitamin D is significantly associated with smell dysfunction independent of aeroallergen sensitization, nasal obstruction, and the presence of allergic rhinitis. This finding may provide insight into the mechanisms involved in the development of olfactory dysfunction.

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