Fluid Intelligence Test Scores Across the Schooling: Evidence of Nonlinear Changes in Girls and Boys

We are incredibly grateful for all participants for their contribution to the study. We thank Tatiana Bykovskaya and Olga Kashubina for their technical support.Received 26 April 2022. Accepted 17 August 2022. Published online 10 October 2022.The results of the analyses of the changes of fluid intelligence scores measured by the Standard Progressive Matrices test across all school years were presented. Sex differences in fluid intelligence scores for each year of schooling as well as in fluid intelligence changes across schooling were analyzed. A total of 1581 participants (51.1% boys) aged 6.8 to 19.1 years from one public school were involved in this cross-sectional study, of whom 871 were primary schoolchildren (mean age = 9.23; range 6.8–11.6), 507 were secondary schoolchildren (mean age = 14.06; range 10.8–18.0), and 203 were high schoolchildren (mean age = 17.25; range 15.3–19.1). To examine the changes in fluid intelligence both correlation analysis and polynomial regression of the total, boys’ and girls’ samples were performed. Linear, quadratic, and cubic regression models were fitted to the data. To explore sex differences in fluid intelligence in each year of schooling, the series of ANOVA were carried out. The results revealed that the school-age change in fluid intelligence is nonlinear for both girls and boys. The changes for girls during the schooling are best described by a quadratic relationship while those for boys are best reflected by a cubic relationship.This work was supported by the Russian Science Foundation under Grant number 17-78-30028

Partner symmetries of the complex Monge-Ampere equation yield hyper-Kahler metrics without continuous symmetries

We extend the Mason-Newman Lax pair for the elliptic complex Monge-Amp\`ere equation so that this equation itself emerges as an algebraic consequence. We regard the function in the extended Lax equations as a complex potential. We identify the real and imaginary parts of the potential, which we call partner symmetries, with the translational and dilatational symmetry characteristics respectively. Then we choose the dilatational symmetry characteristic as the new unknown replacing the K\"ahler potential which directly leads to a Legendre transformation and to a set of linear equations satisfied by a single real potential. This enables us to construct non-invariant solutions of the Legendre transform of the complex Monge-Amp\`ere equation and obtain hyper-K\"ahler metrics with anti-self-dual Riemann curvature 2-form that admit no Killing vectors.Comment: submitted to J. Phys.

Why do spatial abilities predict mathematical performance?

Spatial ability predicts performance in mathematics and eventual expertise in science, technology and engineering. Spatial skills have also been shown to rely on neuronal networks partially shared with mathematics. Understanding the nature of this association can inform educational practices and intervention for mathematical underperformance. Using data on two aspects of spatial ability and three domains of mathematical ability from 4174 pairs of 12-year-old twins, we examined the relative genetic and environmental contributions to variation in spatial ability and to its relationship with different aspects of mathematics. Environmental effects explained most of the variation in spatial ability (~70%) and in mathematical ability (~60%) at this age, and the effects were the same for boys and girls. Genetic factors explained about 60% of the observed relationship between spatial ability and mathematics, with a substantial portion of the relationship explained by common environmental influences (26% and 14% by shared and non-shared environments respectively). These findings call for further research aimed at identifying specific environmental mediators of the spatial–mathematics relationship

Anti-self-dual Riemannian metrics without Killing vectors, can they be realized on K3?

Explicit Riemannian metrics with Euclidean signature and anti-self dual curvature that do not admit any Killing vectors are presented. The metric and the Riemann curvature scalars are homogenous functions of degree zero in a single real potential and its derivatives. The solution for the potential is a sum of exponential functions which suggests that for the choice of a suitable domain of coordinates and parameters it can be the metric on a compact manifold. Then, by the theorem of Hitchin, it could be a class of metrics on $K3$, or on surfaces whose universal covering is $K3$.Comment: Misprints in eqs.(9-11) corrected. Submitted to Classical and Quantum Gravit

Recent advances in genetics of aggressive behavior

One of the most important problems of modern neurobiology and medicine is an understanding of the mechanisms of normal and pathological behavior of a person. Aggressive behavior is an integral part of the human psyche. However, environmental risk factors, mental illness and somatic diseases can lead to increased aggression to be the biological basis of antisocial behavior in a human society. An important role in development of aggressive behavior belongs to the hereditary factors that may be linked to abnormal functioning of neurotransmitter systems in the brain yet the underlying genetic mechanisms remain unclear, which is due to a large number of single nucleotide polymorphisms, insertions and deletions in the structure of genes that encode the components of the neurotransmitter systems. The most studied candidate genes for aggressive behavior are serotonergic (TPH1, TPH2, HTR2A, SLC6A4) and dopaminergic (DRD4, SLC6A3) system genes, as well as the serotonin or catecholamine metabolizing enzyme genes (COMT, MAOA). In addition, there is evidence that the hypothalamic-pituitary system genes (OXT, OXTR, AVPR1A, AVPR1B), the sex hormone receptors genes (ER1, AR), neurotrophin (BDNF) and neuronal apoptosis genes (CASP3, BAX) may also be involved in development of aggressive behavior. The results of Genome-Wide Association Studies (GWAS) have demonstrated that FYN, LRRTM4, NTM, CDH13, DYRK1A and other genes are involved in regulation of aggressive behavior. These and other evidence suggest that genetic predisposition to aggressive behavior may be a very complex process

Longitudinal genetic studies of cognitive characteristics

The present review describes longitudinal studies of cognitive traits and functions determining the causes of their variations and their possible correction to prevent cognitive impairment. The present study reviews the involvement of such environmental factors as nutrition, prenatal maternal stress, social isolation and others in cognitive functioning. The role of epigenetic factors in the implementation of environmental effects in cognitive characteristics is revealed. Considering the epigenome significance, several studies were focused on the design of substances affecting methylation and histone modification, which can be used for the treatment of cognitive disorders. The appropriate correction of epigenetic factors related to environmental differences in cognitive abilities requires to determine the mechanisms of chromatin modifications and variations in DNA methylation. Transposons representing stress-sensitive DNA elements appeared to mediate the environmental influence on epigenetic modifications. They can explain the mechanism of transgenerational transfer of information on cognitive abilities. Recently, large-scale meta-analyses based on the results of studies, which identified genetic associations with various cognitive traits, were carried out. As a result, the role of genes actively expressed in the brain, such as BDNF, COMT, CADM2, CYP2D6, APBA1, CHRNA7, PDE1C, PDE4B, and PDE4D in cognitive abilities was revealed. The association between cognitive functioning and genes, which have been previously involved in developing psychiatric disorders (MEF2C, CYP2D6, FAM109B, SEPT3, NAGA, TCF20, NDUFA6 genes), was revealed, thus indicating the role of the similar mechanisms of genetic and neural networks in both normal cognition and cognitive impairment. An important role in both processes belongs to common epigenetic factors. The genes involved in DNA methylation (DNMT1, DNMT3B, and FTO), histone modifications (CREBBP, CUL4B, EHMT1, EP300, EZH2, HLCS, HUWE1, KAT6B, KMT2A, KMT2D, KMT2C, NSD1, WHSC1, and UBE2A) and chromatin remodeling (ACTB, ARID1A, ARID1B, ATRX, CHD2, CHD7, CHD8, SMARCA2, SMARCA4, SMARCB1, SMARCE1, SRCAP, and SS18L1) are associated with increased risk of psychiatric diseases with cognitive deficiency together with normal cognitive functioning. The data on the correlation between transgenerational epigenetic inheritance of cognitive abilities and the insert of transposable elements in intergenic regions is discussed. Transposons regulate genes functioning in the brain due to the processing of their transcripts into non-coding RNAs. The content, quantity and arrangement of transposable elements in human genome, which do not affect changes in nucleotide sequences of protein encoding genes, but affect their expression, can be transmitted to the next generation

Solutions of the sDiff(2)Toda equation with SU(2) Symmetry

We present the general solution to the Plebanski equation for an H-space that admits Killing vectors for an entire SU(2) of symmetries, which is therefore also the general solution of the sDiff(2)Toda equation that allows these symmetries. Desiring these solutions as a bridge toward the future for yet more general solutions of the sDiff(2)Toda equation, we generalize the earlier work of Olivier, on the Atiyah-Hitchin metric, and re-formulate work of Babich and Korotkin, and Tod, on the Bianchi IX approach to a metric with an SU(2) of symmetries. We also give careful delineations of the conformal transformations required to ensure that a metric of Bianchi IX type has zero Ricci tensor, so that it is a self-dual, vacuum solution of the complex-valued version of Einstein's equations, as appropriate for the original Plebanski equation.Comment: 27 page

Genetic basis of depressive disorders

Depression is a common mental disorder being one of the main causes of disability and mortality worldwide. Despite an intensive research during the past decades, the etiology of depressive disorders (DDs) remains incompletely understood; however, genetic factors are significantly involved in the liability to depression. The present review is focused on the studies based on a candidate gene approach, genome-wide association studies (GWAS) and whole exome sequencing (WES), which previously demonstrated associations between gene polymorphisms and DDs. According to the first approach, DD development is affected by serotonergic (TPH1, TPH2, HTR1A, HTR2A, and SLC6A4), dopaminergic (DRD4, SLC6A3) and noradrenergic (SLC6A2) system genes, and genes of enzymatic degradation (MAOA, COMT). In addition, there is evidence of the involvement of HPA-axis genes (OXTR, AVPR1A, and AVPR1B), sex hormone receptors genes (ESR1, ESR2, and AR), neurotrophin (BDNF) and methylenetetrahydrofolate reductase (MTHFR) genes, neuronal apoptosis (CASP3, BCL-XL, BAX, NPY, APP, and GRIN1) and inflammatory system (TNF, CRP, IL6, IL1B, PSMB4, PSMD9, and STAT3) genes in DD development. The results of the second approach (GWAS and WES) revealed that the PCLO, SIRT1, GNL3, GLT8D1, ITIH3, MTNR1A, BMP5, FHIT, KSR2, PCDH9, and AUTS2 genes predominantly responsible for neurogenesis and cell adhesion are involved in liability to depression. Therefore, the findings discussed suggest that genetic liability to DD is a complex process, which assumes simultaneous functioning of multiple genes including those reported previously, and requires future research in this field

The role of inflammatory system genes in individual differences in nonverbal intelligence

Nonverbal intelligence represents one of the components of brain cognitive functions, which uses visual images and nonverbal approaches for solving required tasks. Interaction between the nervous and immune systems plays a specif ic role in individual differences in brain cognitive functions. Therefore, the genes encoding pro- and antiinf lammatory cytokines are prospective candidate genes in the study of nonverbal intelligence. Within the framework of the present study, we conducted the association analysis of six SNPs in the genes that encode proteins involved in inf lammatory response regulation in the central nervous system (CRP rs3093077, IL1А rs1800587, IL1B rs16944, TNF/ LTA rs1041981, rs1800629, and P2RX7 rs2230912), with nonverbal intelligence in mentally healthy young adults aged 18– 25 years without cognitive decline with inclusion of sex, ethnicity and the presence of the “risky” APOE ε4 allele as covariates. Considering an important role of environmental factors in the development of brain cognitive functions in general and nonverbal intelligence in particular, we conducted an analysis of gene-by-environment (G × E) interactions. As a result of a statistical analysis, rs1041981 and rs1800629 in the tumor necrosis factor gene (TNF) were shown to be associated with a phenotypic variance in nonverbal intelligence at the haplotype level (for АА-haplotype: βST = 1.19; p = 0.033; pperm = 0.047) in carriers of the “risky” APOE ε4 allele. Gene-by-environment interaction models, which determined interindividual differences in nonverbal intelligence, have been constructed: sibship size (number of children in a family) and smoking demonstrated a modulating effect on association of the TNF/LTA (rs1041981) (β = 2.08; βST = 0.16; p = 0.001) and P2RX7 (rs2230912) (β = –1.70; βST = –0.10; p = 0.022) gene polymorphisms with nonverbal intelligence. The data obtained indicate that the effect of TNF/LTA on the development of cognitive functions is evident only in the presence of the “unfavorable” APOE ε4 variant and/or certain environmental conditions

The role of the KIBRA and APOE genes in developing spatial abilities in humans

In the contemporary high-tech society, spatial abilities predict individual life and professional success, especially in the STEM (Science, Technology, Engineering, and Mathematics) disciplines. According to neurobiological hypotheses, individual differences in cognitive abilities may be attributed to the functioning of genes involved in the regulation of neurogenesis and synaptic plasticity. In addition, genome-wide association studies identified rs17070145 located in the KIBRA gene, which was associated with individual differences in episodic memory. Considering a significant role of genetic and environmental components in cognitive functioning, the present study aimed to estimate the main effect of NGF (rs6330), NRXN1 (rs1045881, rs4971648), KIBRA (rs17070145), NRG1 (rs6994992), BDNF (rs6265), GRIN2B (rs3764030), APOE (rs7412, rs429358), and SNAP25 (rs363050) gene polymorphisms and to assess the effect of gene-environment interactions on individual differences in spatial ability in individuals without cognitive decline aged 18–25 years (N = 1011, 80 % women). Spatial abilities were measured using a battery of cognitive tests including the assessment of “3D shape rotation” (mental rotation). Multiple regression analysis, which was carried out in the total sample controlling for sex, ethnicity and the presence of the “risk” APOE ε4 allele, demonstrated the association of the rs17070145 Т-allele in the KIBRA gene with enhanced spatial ability (β = 1.32; pFDR = 0.037) compared to carriers of the rs17070145 CC-genotype. The analysis of gene-environment interactions revealed that nicotine smoking (β = 3.74; p = 0.010) and urban/rural residency in childhood (β = –6.94; p = 0.0002) modulated the association of KIBRA rs17070145 and АРОЕ (rs7412, rs429358) gene variants with individual differences in mental rotation, respectively. The data obtained confirm the effect of the KIBRA rs17070145 Т-allele on improved cognitive functioning and for the first time evidence the association of the mentioned genetic variant with spatial abilities in humans. A “protective” effect of the APOE ε2 allele on enhanced cognitive functioning is observed only under certain conditions related to childhood rearing