Multiple studies have reported that individuals with low birth weights (LBW, <2500 g) have a lower intelligence quotient (IQ) than those with normal birth weights (NBW, ≥2500 g). Based on 57 eligible individual studies including 12,137 participants, we performed a meta-analysis to estimate the association between low birth weight and individuals’ IQ scores (IQs). The pooled weight mean difference (WMD) in IQs between NBW and LBW individuals was 10 (95% CI 9.26–11.68). The WMD was stable regardless of age. No publication bias was detected. The mean IQs of the extremely low birth weight (ELBW, <1000 g), very low birth weight (VLBW, 1000–1499 g), moderately low birth weight (MLBW, 1500–2499 g) and NBW individuals were 91, 94, 99 and 104, respectively. Additionally, the WMD in IQs with NBW were 14, 10 and 7 for ELBW, VLBW, and MLBW individuals, respectively. Two studies permitted estimates of the influence of social determinants of health to the discrepancy in IQs, which was 13%. Since IQ is inherited and influenced by environmental factors, parental IQs and other factors contribute to residual confounding of the results. As the conclusion was based on population studies, it may not be applicable to a single individual.

Increasing evidence suggests that abnormal synaptic function leads to neuronal developmental disorders and is an important component of the etiology of autism spectrum disorder (ASD). Neurexins are presynaptic cell-adhesion molecules that affect the function of synapses and mediate the conduction of nerve signals. Thus, neurexins are attractive candidate genes for autism. Since gene families have greater power to reveal genetic association than single genes, we designed this case-control study to investigate six genetic variants in three neurexin genes (NRXN1, NRXN2, and NRXN3) in a Chinese population including 529 ASD patients and 1,923 healthy controls. We found that two SNPs were significantly associated with ASD after false discovery rate (FDR) adjustment for multiple comparisons. The NRXN2 rs12273892 polymorphism T allele and AT genotype were significantly associated with increased risk of ASD (respectively: OR 5 1.328, 95% CI 5 1.133-1.557, P < 0.001; OR 5 1.528; 95% CI 5 1.249-1.868, P < 0.001). The dominant model showed the same association (OR 5 1.495, 95% CI 5 1.231-1.816, P < 0.001). The NRXN3 rs12879016 polymorphism played a significant role in ASD susceptibility under the dominant model (OR 5 0.747, 95% CI5 0.615-0.908, P 5 0.023), with the same trend detected for the G allele and GT genotype (respectively: OR 5 0.811, 95% CI 5 0.699-0.941, P 5 0.036; OR 5 0.755, 95% CI 5 0.615-0.928, P 5 0.035). In conclusion, this study supports the importance of two genetic variants in the neurexin gene family in ASD susceptibility in China. Autism Res 2018, 11: 37-43. V C 2017 International Society for Autism Research, Wiley Periodicals, Inc.Lay Summary: Autism spectrum disorder (ASD) is a neurodevelopmental disorder that is highly heritable, and studies have found a number of candidate genes that might contribute to ASD. Neurexins are presynaptic cell-adhesion molecules that affect the function of synapses and mediate the conduction of nerve signals, and they play an important role in normal brain development and become candidate genes for autism. The purpose of our study is to explore the association between variants of the neurexins gene family and ASD in a Chinese population through a case-control study.

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BackgroundIt is well known that males have a higher prevalence of developmental dyslexia (DD) than females. Although the mechanism underlying this gender difference remains unknown, the contactin-associated protein-like 2 (CNTNAP2) gene, which shows sex-specific patterns in some neurodevelopmental disorders, has attracted extensive attention. This study aimed to explore whether CNTNAP2 shows a sex-specific association with DD in a Chinese population.MethodsUsing genomic DNA samples of 726 students [372 cases (282 male, 90 female), 354 controls (267 male, 87 female)], we genotyped five SNPs of CNTNAP2. Gender-stratified logistic regression models were used to determine the relationships between the CNTNAP2 variants and DD.FindingsAfter adjustment for the false discovery rate (FDR), two SNPs (rs3779031, rs987456) of CNTNAP2 were associated with DD risk in females but not in males. Female participants carrying the rs3779031 G allele had a lower risk of DD than those with the A genotype [GG vs AA: OR (95%CI) = 0.281 (0.097–0.814)]. The rs987456 CC genotype was associated with a decreased risk of DD in females [CC vs AA+CA: OR (95%CI) = 0.222 (0.078–0.628)]. Furthermore, the interaction between CNTNAP2 (rs987456) and environmental factors (scheduled reading time) played a protective role in females [OR (95%CI) = 0.431 (0.188–0.987)].InterpretationWe performed a genetic association study on CNTNAP2 variants and DD. The sex specificity of CNTNAP2 in DD, along with the gene-environment interaction may help us to understand gender differences in DD.