Abstract
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.
Highlights
Stability and variability of cognitive abilities in ontogenesis Recently, in addition to highly informative methods of molecular biological research used for the identification of specific genetic loci involved in cognitive functioning at the genomewide level, studies on the detection of genetic determinants under the longitudinal paradigm have become of great importance
An elevated maternal cortisol level at the end of pregnancy was associated with higher cognitive development and performance at the age of 12 months. These results suggest that maternal cortisol and pregnancy-specific anxiety have a programmed effect on the developing fetus, which can be mediated by epigenetic factors (Davis, Sandman, 2010)
Longitudinal studies proved that an increasing phenotypic stability in cognitive abilities in human development was mediated by genetic factors
Summary
Longitudinal studies make it possible to obtain specific objective data on dynamics and to evaluate the contribution of genetic and environmental factors to the changes in cognitive differences in human ontogenesis. A large-scale meta-analysis based on the results of 16 longitudinal studies examining the role of genetic and environmental components in cognitive functioning in 11,500 pairs of twins and siblings assessed twice within the period from 6 months to 18 years, revealed that in early childhood innovative adaptation effects prevail as a response to novel environmental stimuli and rapidly decrease by adolescence.
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