Hemispheric asymmetry is a fundamental organizing principle of the human brain. Answering the genetic effects of the asymmetry is a prerequisite for elucidating developmental mechanisms of brain asymmetries. Multi-modal magnetic resonance imaging (MRI) has provided an important tool for comprehensively interpreting human brain asymmetry and its genetic mechanism. By combining MRI data, individual differences in brain structural asymmetry have been investigated with quantitative genetic brain mapping using gene-heritability. Twins provide a useful natural model for studying the effects of genetics and environment on the brain. Studies based on MRI have found that the asymmetry of human brain structure has a genetic basis. From the perspective of quantitative genetic analysis, this article reviews recent findings on the genetic effects of asymmetry and genetic covariance between hemispheres from three aspects: the asymmetry of heritability, the heritability of asymmetry and the genetic correlation. At last, the article shows the limitations and future research directions in this field. The purpose of this systematic review is to quickly guide researchers to understand the origins and genetic mechanism of interhemispheric differences, and provide a genetic basis for further understanding and exploring individual differences in laterized cognitive behavior.
Objective To explore the shared genetic structure and causal relationship between respiratory diseases and obstructive sleep apnea (OSA) through comprehensive genetic analysis. Methods In this study, we utilized large-scale genome-wide association studies (GWAS) summary statistics and novel statistical genetic approaches. We incorporated genetic data related to respiratory diseases to align with OSA. We conducted a genome-wide cross-trait analysis to assess genetic correlation, identify shared loci, examine expression-trait associations, and infer causal relationships. Results We found positive genetic correlation between acute upper respiratory infections and OSA (rg=0.435, P=3.47×10?14), acute lower respiratory infections and OSA (rg=0.481, P=4.03×10?5), acute bronchitis and OSA (rg=0.453, P=7.00×10?4), pneumonia and OSA (rg=0.368, P=7.94×10?10), asthma and OSA (rg=0.364, P=2.73×10?19), and COPD and OSA (rg=0.300, P=1.10×10?10). We conducted a cross-trait meta-analysis to identify shared loci between respiratory diseases and OSA. Additionally, we employed summary-based Mendelian randomization (SMR) to predict causal genes associated with both respiratory diseases and OSA. Mendelian randomization (MR) supported the causal roles of pneumonia (IVW OR=1.15; 95%CI 1.02-1.30), asthma (IVW OR=1.05, 95%CI 1.01-1.08) in OSA, while not observe any significant association between other respiratory diseases and the risk of OSA. Conclusions An intrinsic link between respiratory diseases and OSA has been demonstrated. The genetic correlation and causal role of respiratory diseases in OSA emphasize the importance of considering respiratory health in the management of OSA.
