Alterations in resting-state networks (RSNs) are often associated with psychiatric and neurologic disorders. Given this critical linkage, it has been hypothesized that RSNs can potentially be used as endophenotypes for brain diseases. To validate this notion, a critical step is to show that RSNs exhibit heritability. However, the investigation of the genetic basis of RSNs has only been attempted in the default-mode network at the region-of-interest level, while the genetic control on other RSNs has not been determined yet. Here we examined the genetic and environmental influences on eight well-characterized RSNs by using a twin design. Resting-state functional magnetic resonance imaging data in 56 pairs of twins were collected. The genetic and environmental effects on each RSN were estimated by fitting the functional connectivity covariance of each voxel in the RSN to the classic ACE twin model. The data showed that although environmental effects accounted for the majority of variance in widespread areas, there were specific brain sites that showed significant genetic control for individual RSNs. These results suggest that part of the human brain functional connectome is shaped by genomic constraints. Importantly, this information can be useful for bridging genetic analysis and network-level assessment of brain disorders.

Background Internet addiction has become a major global concern and a burden on mental health. However, there is a lack of consensus on its link to mental health outcomes. Objective The aim of this study was to investigate the associations between internet addiction severity and adverse mental health outcomes. Methods First-year undergraduates enrolled at Sichuan University during September 2015, 2016, 2017, and 2018 were invited to participate in the current study survey, 85.13% (31,659/37,187) of whom fully responded. Young’s 20-item Internet Addiction Test, Patient Health Questionnaire-15, Patient Health Questionnaire-9, Symptom Checklist 90, Six-Item Kessler Psychological Distress Scale, and Suicidal Behaviors Questionnaire-Revised were used to evaluate internet addiction, four psychopathologies (high somatic symptom severity, clinically significant depression, psychoticism, and paranoia), serious mental illness, and lifetime suicidality. Results The prevalence of students with mild, moderate, and severe internet addiction was 37.93% (12,009/31,659), 6.33% (2003/31,659), and 0.20% (63/31,659), respectively. The prevalence rates of high somatic symptom severity, clinically significant depression, psychoticism, paranoid ideation, and serious mental illness were 6.54% (2072/31,659), 4.09% (1294/31,659), 0.51% (160/31,659), 0.52% (165/31,659), and 1.88% (594/31,659), respectively, and the lifetime prevalence rates of suicidal ideation, suicidal plan, and suicidal attempt were 36.31% (11,495/31,659), 5.13% (1624/31,659), and 1.00% (315/31,659), respectively. The prevalence rates and odds ratios (ORs) of the four psychopathologies and their comorbidities, screened serious mental illness, and suicidalities in the group without internet addiction were much lower than the average levels of the surveyed population. Most of these metrics in the group with mild internet addiction were similar to or slightly higher than the average rates; however, these rates sharply increased in the moderate and severe internet addiction groups. Among the four psychopathologies, clinically significant depression was most strongly associated with internet addiction after adjusting for the confounding effects of demographics and other psychopathologies, and its prevalence increased from 1.01% (178/17,584) in the students with no addiction to 4.85% (582/12,009), 24.81% (497/2,003), and 58.73% (37/63) in the students with mild, moderate, and severe internet addiction, respectively. The proportions of those with any of the four psychopathologies increased from 4.05% (713/17,584) to 11.72% (1408/12,009), 36.89% (739/2003), and 68.25% (43/63); those with lifetime suicidal ideation increased from 24.92% (4382/17,584) to 47.56% (5711/12,009), 67.70% (1356/2003), and 73.02% (46/63); those with a suicidal plan increased from 2.59% (456/17,584) to 6.77% (813/12,009), 16.72% (335/2003), and 31.75% (20/63); and those with a suicidal attempt increased from 0.50% (88/17,584) to 1.23% (148/12,009), 3.54% (71/2003), and 12.70% (8/63), respectively. Conclusions Moderate and severe internet addiction were strongly associated with a broad group of adverse mental health outcomes, including somatic symptoms that are the core features of many medical illnesses, although clinically significant depression showed the strongest association. This finding supports the illness validity of moderate and severe internet addiction in contrast to mild internet addiction. These results are important for informing health policymakers and service suppliers from the perspective of resolving the overall human health burden in the current era of “Internet Plus” and artificial intelligence.

A complete characterization of genetic variation is a fundamental goal of human genome research. Long-read sequencing has improved the sensitivity of structural variant discovery. Here, we conduct the long-read sequencing-based structural variant analysis for 405 unrelated Chinese individuals, with 68 phenotypic and clinical measurements. We discover a landscape of 132,312 nonredundant structural variants, of which 45.2% are novel. The identified structural variants are of high-quality, with an estimated false discovery rate of 3.2%. The concatenated length of all the structural variants is approximately 13.2% of the human reference genome. We annotate 1,929 loss-of-function structural variants affecting the coding sequence of 1,681 genes. We discover rare deletions in HBA1/HBA2/HBB associated with anemia. Furthermore, we identify structural variants related to immunity which differentiate the northern and southern Chinese populations. Our study describes the landscape of structural variants in the Chinese population and their contribution to phenotypes and disease.

There is compelling evidence that epigenetic factors contribute to the manifestation of depression, in which microRNA132 (miR-132) is suggested to play a pivotal role in the pathogenesis and neuronal mechanisms underlying the symptoms of depression. Additionally, several depression-associated genes [MECP2, ARHGAP32 (p250GAP), CREB, and period genes] were experimentally validated as miR-132 targets. However, most studies regarding miR-132 in major depressive disorder are based on post-mortem, animal models or genetic comparisons. This work will be the first attempt to investigate how miR-132 dysregulation may impact covariation of multimodal brain imaging data in 81 unmedicated major depressive patients and 123 demographically-matched healthy controls, as well as in a medication-naïve subset of major depressive patients. MiR-132 values in blood (patients > controls) was used as a prior reference to guide fusion of three MRI features: fractional amplitude of low frequency fluctuations, grey matter volume, and fractional anisotropy. The multimodal components correlated with miR-132 also show significant group difference in loadings. Results indicate that (i) higher miR-132 levels in major depressive disorder are associated with both lower fractional amplitude of low frequency fluctuations and lower grey matter volume in fronto-limbic network; and (ii) the identified brain regions linked with increased miR-132 levels were also associated with poorer cognitive performance in attention and executive function. Using a data-driven, supervised-learning method, we determined that miR-132 dysregulation in major depressive disorder is associated with multi-facets of brain function and structure in fronto-limbic network (the key network for emotional regulation and memory), which deepens our understanding of how miR-132 dysregulation in major depressive disorders contribute to the loss of specific brain areas and is linked to relevant cognitive impairments.