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"Intelligence - genetics"
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The singularity is nearer : when we merge with Al
\"This successor volume to The Singularity Is Near explores how technology will refashion the human race in the decades to come. In this entirely new book, Ray Kurzweil brings a fresh perspective to advances in the singularity-assessing the progress of many of his predictions and examining the novel advancements that, in the near future, will bring a revolution in knowledge and an expansion of human potential. Among the topics he discusses are rebuilding the world atom by atom with devices like nanobots; radical life extension beyond the current age limit of 120; reinventing intelligence by expanding biological capacity with nonbiological intelligence in the cloud; how life is improving with declines in poverty and violence; and the growth of technologies that can be applied to everything from clothes to building materials to growing human organs. He also considers the potential perils of biotechnology, nanotechnology, and artificial intelligence, including such topics as how AI will impact unemployment and the safety of autonomous cars, and \"After Life\" technology, which will reanimate people who have passed away through a combination of data and DNA\"-- Provided by publisher.
Book
Overlap Between the General Factor of Personality and Trait Emotional Intelligence: A Genetic Correlation Study
A previous meta-analysis (Van der Linden et al., Psychol Bull 143:36–52, 2017) showed that the General Factor of Personality (GFP) overlaps with ability as well as trait emotional intelligence (EI). The correlation between trait EI and the GFP was so high (ρ = 0.88) in that meta-analysis that these two may be considered virtually identical constructs. The present study builds on these findings by examining whether the strong phenotypic correlation between the GFP and trait EI has a genetic component. In a sample of monozygotic and dizygotic twins, the heritability estimates for the GFP and trait EI were 53 and 45%, respectively. Moreover, there was a strong genetic correlation of r = .90 between the GFP and trait EI. Additional analyses suggested that a substantial proportion of the genetic correlations reflects non-additive genetic effects (e.g., dominance and epistasis). These findings are discussed in light of evolutionary accounts of the GFP.
Journal Article
Genetic predictors of educational attainment and intelligence test performance predict voter turnout
Although the genetic influence on voter turnout is substantial (typically 40–50%), the underlying mechanisms remain unclear. Across the social sciences, research suggests that ‘resources for politics’ (as indexed notably by educational attainment and intelligence test performance) constitute a central cluster of factors that predict electoral participation. Educational attainment and intelligence test performance are heritable. This suggests that the genotypes that enhance these phenotypes could positively predict turnout. To test this, we conduct a genome-wide complex trait analysis of individual-level turnout. We use two samples from the Danish iPSYCH case–cohort study, including a nationally representative sample as well as a sample of individuals who are particularly vulnerable to political alienation due to psychiatric conditions (
n
= 13,884 and
n
= 33,062, respectively). Using validated individual-level turnout data from the administrative records at the polling station, genetic correlations and Mendelian randomization, we show that there is a substantial genetic overlap between voter turnout and both educational attainment and intelligence test performance.
The genetic variance that predicts educational attainment or intelligence test performance predicts individual-level voter turnout in a nationally representative sample and among people with psychiatric conditions, such as depression.
Journal Article
Common genetic variants contribute to risk of rare severe neurodevelopmental disorders
There are thousands of rare human disorders that are caused by single deleterious, protein-coding genetic variants
1
. However, patients with the same genetic defect can have different clinical presentations
2
–
4
, and some individuals who carry known disease-causing variants can appear unaffected
5
. Here, to understand what explains these differences, we study a cohort of 6,987 children assessed by clinical geneticists to have severe neurodevelopmental disorders such as global developmental delay and autism, often in combination with abnormalities of other organ systems. Although the genetic causes of these neurodevelopmental disorders are expected to be almost entirely monogenic, we show that 7.7% of variance in risk is attributable to inherited common genetic variation. We replicated this genome-wide common variant burden by showing, in an independent sample of 728 trios (comprising a child plus both parents) from the same cohort, that this burden is over-transmitted from parents to children with neurodevelopmental disorders. Our common-variant signal is significantly positively correlated with genetic predisposition to lower educational attainment, decreased intelligence and risk of schizophrenia. We found that common-variant risk was not significantly different between individuals with and without a known protein-coding diagnostic variant, which suggests that common-variant risk affects patients both with and without a monogenic diagnosis. In addition, previously published common-variant scores for autism, height, birth weight and intracranial volume were all correlated with these traits within our cohort, which suggests that phenotypic expression in individuals with monogenic disorders is affected by the same variants as in the general population. Our results demonstrate that common genetic variation affects both overall risk and clinical presentation in neurodevelopmental disorders that are typically considered to be monogenic.
A genome-wide association study of approximately 7,000 patients with neurodevelopmental disorders demonstrates that overall risk and clinical presentation in putative monogenic disorders is also influenced by common genetic variants present in the general population.
Journal Article
The new genetics of intelligence
Intelligence -- the ability to learn, reason and solve problems -- is at the forefront of behavioural genetic research. Intelligence is highly heritable and predicts important educational, occupational and health outcomes better than any other trait. Recent genome-wide association studies have successfully identified inherited genome sequence differences that account for 20% of the 50% heritability of intelligence. These findings open new avenues for research into the causes and consequences of intelligence using genome-wide polygenic scores that aggregate the effects of thousands of genetic variants.
Journal Article
Polygenic transmission disequilibrium confirms that common and rare variation act additively to create risk for autism spectrum disorders
Elise Robinson and colleagues present the polygenic transmission disequilibrium test (pTDT) for evaluating transmission of polygenic risk in family-based study designs. The authors apply pTDT to a cohort of autism spectrum disorder (ASD) families and find that common polygenic variation acts additively with
de novo
variants to contribute to ASD risk.
Autism spectrum disorder (ASD) risk is influenced by common polygenic and
de novo
variation. We aimed to clarify the influence of polygenic risk for ASD and to identify subgroups of ASD cases, including those with strongly acting
de novo
variants, in which polygenic risk is relevant. Using a novel approach called the polygenic transmission disequilibrium test and data from 6,454 families with a child with ASD, we show that polygenic risk for ASD, schizophrenia, and greater educational attainment is over-transmitted to children with ASD. These findings hold independent of proband IQ. We find that polygenic variation contributes additively to risk in ASD cases who carry a strongly acting
de novo
variant. Lastly, we show that elements of polygenic risk are independent and differ in their relationship with phenotype. These results confirm that the genetic influences on ASD are additive and suggest that they create risk through at least partially distinct etiologic pathways.
Journal Article
Genome-wide association meta-analysis in 269,867 individuals identifies new genetic and functional links to intelligence
Intelligence is highly heritable
1
and a major determinant of human health and well-being
2
. Recent genome-wide meta-analyses have identified 24 genomic loci linked to variation in intelligence
3
–
7
, but much about its genetic underpinnings remains to be discovered. Here, we present a large-scale genetic association study of intelligence (
n
= 269,867), identifying 205 associated genomic loci (190 new) and 1,016 genes (939 new) via positional mapping, expression quantitative trait locus (eQTL) mapping, chromatin interaction mapping, and gene-based association analysis. We find enrichment of genetic effects in conserved and coding regions and associations with 146 nonsynonymous exonic variants. Associated genes are strongly expressed in the brain, specifically in striatal medium spiny neurons and hippocampal pyramidal neurons. Gene set analyses implicate pathways related to nervous system development and synaptic structure. We confirm previous strong genetic correlations with multiple health-related outcomes, and Mendelian randomization analysis results suggest protective effects of intelligence for Alzheimer’s disease and ADHD and bidirectional causation with pleiotropic effects for schizophrenia. These results are a major step forward in understanding the neurobiology of cognitive function as well as genetically related neurological and psychiatric disorders.
Meta-analysis of genome-wide association studies for cognitive ability identifies 190 new loci and implicates 939 new genes related to neurogenesis, neuron differentiation and synaptic structure.
Journal Article
Genetics and intelligence differences: five special findings
Intelligence is a core construct in differential psychology and behavioural genetics, and should be so in cognitive neuroscience. It is one of the best predictors of important life outcomes such as education, occupation, mental and physical health and illness, and mortality. Intelligence is one of the most heritable behavioural traits. Here, we highlight five genetic findings that are special to intelligence differences and that have important implications for its genetic architecture and for gene-hunting expeditions. (i) The heritability of intelligence increases from about 20% in infancy to perhaps 80% in later adulthood. (ii) Intelligence captures genetic effects on diverse cognitive and learning abilities, which correlate phenotypically about 0.30 on average but correlate genetically about 0.60 or higher. (iii) Assortative mating is greater for intelligence (spouse correlations ~0.40) than for other behavioural traits such as personality and psychopathology (~0.10) or physical traits such as height and weight (~0.20). Assortative mating pumps additive genetic variance into the population every generation, contributing to the high narrow heritability (additive genetic variance) of intelligence. (iv) Unlike psychiatric disorders, intelligence is normally distributed with a positive end of exceptional performance that is a model for ‘positive genetics’. (v) Intelligence is associated with education and social class and broadens the causal perspectives on how these three inter-correlated variables contribute to social mobility, and health, illness and mortality differences. These five findings arose primarily from twin studies. They are being confirmed by the first new quantitative genetic technique in a century—Genome-wide Complex Trait Analysis (GCTA)—which estimates genetic influence using genome-wide genotypes in large samples of unrelated individuals. Comparing GCTA results to the results of twin studies reveals important insights into the genetic architecture of intelligence that are relevant to attempts to narrow the ‘missing heritability’ gap.
Journal Article
Genome-wide detection of tandem DNA repeats that are expanded in autism
Tandem DNA repeats vary in the size and sequence of each unit (motif). When expanded, these tandem DNA repeats have been associated with more than 40 monogenic disorders
1
. Their involvement in disorders with complex genetics is largely unknown, as is the extent of their heterogeneity. Here we investigated the genome-wide characteristics of tandem repeats that had motifs with a length of 2–20 base pairs in 17,231 genomes of families containing individuals with autism spectrum disorder (ASD)
2
,
3
and population control individuals
4
. We found extensive polymorphism in the size and sequence of motifs. Many of the tandem repeat loci that we detected correlated with cytogenetic fragile sites. At 2,588 loci, gene-associated expansions of tandem repeats that were rare among population control individuals were significantly more prevalent among individuals with ASD than their siblings without ASD, particularly in exons and near splice junctions, and in genes related to the development of the nervous system and cardiovascular system or muscle. Rare tandem repeat expansions had a prevalence of 23.3% in children with ASD compared with 20.7% in children without ASD, which suggests that tandem repeat expansions make a collective contribution to the risk of ASD of 2.6%. These rare tandem repeat expansions included previously undescribed ASD-linked expansions in
DMPK
and
FXN
, which are associated with neuromuscular conditions, and in previously unknown loci such as
FGF14
and
CACNB1
. Rare tandem repeat expansions were associated with lower IQ and adaptive ability. Our results show that tandem DNA repeat expansions contribute strongly to the genetic aetiology and phenotypic complexity of ASD.
Genome-wide analysis of tandem DNA repeats in the genomes of individuals with autism spectrum disorder and control participants reveals a strong contribution of tandem repeat expansions to the genetic aetiology and phenotypic complexity of autism spectrum disorder.
Journal Article