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It is now possible to create individual-specific genetic scores, called genome-wide polygenic scores (GPS). We used a GPS for years of education ("EduYears") to predict reading performance assessed at UK National Curriculum Key Stages 1 (age 7), 2 (age 12) and 3 (age 14) and on reading tests administered at ages 7 and 12 in a UK sample of 5,825 unrelated individuals. "EduYears" GPS accounts for up to 5% of the variance in reading performance at age 14. GPS predictions remained significant after accounting for general cognitive ability and family socioeconomic status. Reading performance of children in the lowest and highest 12.5% of the "EduYears" GPS distribution differed by a mean growth in reading ability of approximately two school years. It seems certain that polygenic scores will be used to predict strengths and weaknesses in education.

This first Japanese twin study of early literacy development investigated the extent to which genetic and environmental factors influence individual differences in prereading skills in 238 pairs of twins at 42 months of age. Twin pairs were individually tested on measures of phonological awareness, "kana" letter name/sound knowledge, receptive vocabulary, visual perception, nonword repetition, and digit span. Results obtained from univariate behavioral-genetic analyses yielded little evidence for genetic influences, but substantial shared-environmental influences, for all measures. Phenotypic confirmatory factor analysis suggested three correlated factors: phonological awareness, letter name/sound knowledge, and general prereading skills. Multivariate behavioral genetic analyses confirmed relatively small genetic and substantial shared environmental influences on the factors. The correlations among the three factors were mostly attributable to shared environment. Thus, shared environmental influences play an important role in the early reading development of Japanese children. (Contains 7 tables and 1 figure.)

Identical and fraternal twins (N = 540, age 8 to 18 years) were tested on three different measures of writing (Woodcock-Johnson III Tests of Achievement--Writing Samples and Writing Fluency; Handwriting Copy from the Group Diagnostic Reading and Aptitude Achievement Tests), three different language skills (phonological awareness, rapid naming, and vocabulary), and three different reading skills (word recognition, spelling, and reading comprehension). Substantial genetic influence was found on two of the writing measures, writing samples and handwriting copy, and all of the language and reading measures. Shared environment influences were generally not significant, except for Vocabulary. Non-shared environment estimates, including measurement error, were significant for all variables. Genetic influences among the writing measures were significantly correlated (highest between the speeded measures writing fluency and handwriting copy), but there were also significant independent genetic influences between copy and samples and between fluency and samples. Genetic influences on writing were significantly correlated with genetic influences on all of the language and reading skills, but significant independent genetic influences were also found for copy and samples, whose genetic correlations were significantly less than 1.0 with the reading and language skills. The genetic correlations varied significantly in strength depending on the overlap between the writing, language, and reading task demands. We discuss implications of our results for education, limitations of the study, and new directions for research on writing and its relations to language and reading.

Genetic and environmental relations between vocabulary and reading skills were explored longitudinally from preschool through Grades 2 and 4. At preschool there were strong shared-environment and weak genetic influences on both vocabulary and print knowledge but substantial differences in their source. Separation of etiology for vocabulary and reading continued for word recognition and decoding through Grade 4, but genetic and environmental correlations between vocabulary and reading comprehension approached unity by Grade 4, when vocabulary and word recognition accounted for all of the genetic and shared environment influences on reading comprehension. (Contains 7 tables.)

Does the choice of test for assessing reading comprehension influence the outcome of genetic analyses? A twin design compared two types of reading comprehension tests classified as primarily associated with word decoding (RC-D) or listening comprehension (RC-LC). For both types of tests, the overall genetic influence is high and nearly identical. However, the tests differed significantly in how they covary with the genes associated with decoding and listening comprehension. Although Cholesky decomposition showed that both types of comprehension tests shared significant genetic influence with both decoding and listening comprehension, RC-D tests shared most genetic variance with decoding, and RC-LC tests shared most with listening comprehension. Thus, different tests used to measure the same construct may manifest very different patterns of genetic covariation. These results suggest that the apparent discrepancies among the findings of previous twin studies of reading comprehension could be due at least in part to test differences. (Contains 5 tables, 1 figure and 1 footnote.)

As part of a longitudinal twin study of literacy and language, we conducted a behaviour-genetic analysis of orthographic learning, spelling and decoding in Grade 2 children (225 identical and 214 fraternal twin pairs) in the United States and Australia. Each variable showed significant genetic and unique environment influences. Multivariate analyses revealed very high genetic correlations among the variables, indicating that the same genes are involved in their aetiology. These genes are partly independent of those contributing to intelligence. A further analysis indicated that the covariation between decoding and orthographic learning is mediated by shared genes rather than by a direct causal path. The authors argue that a learning parameter, most directly assessed by orthographic learning in this study, underlies all three literacy variables. The results are also discussed in relation to Share's self-teaching hypothesis, which may require modification.

Genetic and environmental influences on early reading and spelling at the end of kindergarten and Grade 1 were compared across three twin samples tested in the United States, Australia, and Scandinavia. Proportions of variance due to genetic influences on kindergarten reading were estimated at 0.84 in Australia, 0.68 in the U.S., and 0.33 in Scandinavia. The effects of shared environment on kindergarten reading were estimated at 0.09 in Australia, 0.25 in the U.S., and 0.52 in Scandinavia. A similar pattern of genetic and environmental influences was obtained for kindergarten spelling. One year later when twins in all three samples had received formal literacy instruction for at least one full school year, heritability was similarly high across country, with estimated genetic influences varying between 0.79 and 0.83 for reading and between 0.62 and 0.79 for spelling. These findings indicate that the pattern of genetic and environmental influences on early reading and spelling development varies according to educational context, with genetic influence increasing as a function of increasing intensity of early instruction. Longitudinal analyses revealed genetic continuity for both reading and spelling between kindergarten and Grade 1 across country. However, a new genetic factor comes into play accounting for independent variance in reading at Grade 1 in the U.S. and Scandinavia, suggesting a change in genetic influences on reading. Implications for response-to-instruction are discussed. (Contains 7 tables.)

The primary objectives of the present study are to introduce the Colorado Longitudinal Twin Study of Reading Disability, the first longitudinal twin study in which subjects have been specifically selected for having a history of reading difficulties, and to present some initial assessments of the stability of reading performance and cognitive abilities in this sample. Preliminary examination of the test scores of 124 twins with a history of reading difficulties and 154 twins with no history of reading difficulties indicates that over the 5- to 6-year interval between assessments, cognitive and reading performance are highly stable. As a group, those subjects with a history of reading difficulties had substantial deficits relative to control subjects on all measures at initial assessment, and significant deficits remained at follow-up. The stability noted for all cognitive and achievement measures was highest for a composite measure of reading, whose average stability correlation across groups was 0.80. Results of preliminary behavior genetic analyses for this measure indicated that shared genetic influences accounted for 86% and 49% of the phenotypic correlations between the two assessments for twin pairs with and without reading difficulties, respectively. In addition, genetic correlations reached unity for both groups, suggesting that the same genetic influences are manifested at both time points.

Grade 1 literacy skills of twin children in Australia (New South Wales) and the United States (Colorado) were explored in a genetically sensitive design (N = 319 pairs). Analyses indicated strong genetic influence on word and nonword identification, reading comprehension, and spelling. Rapid naming showed more modest, though reliable, genetic influence. Phonological awareness was subject to high nonshared environment and no reliable genetic effects, and individual measures of memory and learning were also less affected by genes than nonshared environment. Multivariate analyses showed that the same genes affected word identification, reading comprehension, and spelling. Country comparisons indicated that the patterns of genetic influence on reading and spelling in Grade 1 were similar, though for the U.S. but not the Australian children new genes came on stream in the move from kindergarten to Grade 1. We suggest that this is because the more intensive kindergarten literacy curriculum in New South Wales compared with Colorado, consistent with the mean differences between the two countries, means that more of the genes are "online" sooner in Australia because of accelerated overall reading development.

Genetic and environmental influences on prereading skills in preschool and on early reading and spelling development at the end of kindergarten were compared among samples of identical and fraternal twins from the U.S. (Colorado), Australia, and Scandinavia. Mean comparisons revealed significantly lower preschool print knowledge in Scandinavia, consistent with the relatively lower amount of shared book reading and letter-based activities with parents, and lack of emphasis on print knowledge in Scandinavian preschools. The patterns of correlations between all preschool environment measures and prereading skills within the samples were remarkably similar, as were the patterns of genetic, shared environment, and non-shared environment estimates: in all samples, genetic influence was substantial and shared environment influence was relatively weak for phonological awareness, rapid naming, and verbal memory; genetic influence was weak, and shared environment influence was relatively strong for vocabulary and print knowledge. In contrast, for reading and spelling assessed at the end of kindergarten in the Australian and U.S. samples, there was some preliminary evidence for country differences in the magnitude of genetic and environmental influences. We argue that the apparently higher genetic and lower shared environment influence in the Australian sample was related to a greater emphasis on formal reading instruction, resulting in more advanced reading and spelling skills at the end of kindergarten, and thus there was greater opportunity to observe genetic influences on response to systematic reading instruction among the Australian twins.

To test the hypothesis that the etiology of reading difficulties may differ for males and females in more severely impaired samples, reading performance data from monozygotic (MZ), same-sex dizygotic (DZ[subscript ss]), and opposite-sex dizygotic (DZ[subscript os]) twin pairs were analyzed using a model-fitting implementation of the DeFries-Fulker (DF) model (Purcell & Sham, 2003, "Behavior genetics", 33, 271-278). Five non-independent samples were selected using cut-offs of -1 (N = 737 pairs), -1.5 (N = 654), -2 (N = 468), -2.5 (N = 335), and -3 (N = 198) standard deviations (s) below the mean composite reading score of control twins. Male/female gender ratios for children with reading difficulties were significantly higher than 1.0 for all five samples and increased as a function of severity (viz., 1.15, 1.17, 1.40, 1.61, and 1.88, respectively). When the DF model was fit to the data, estimates of heritability (h[subscript g [squared]] ) and shared environmental influences (c[subscript g [squared]] ) were not significantly different for males and females in any of the groups. Consequently, the most parsimonious model that provided a good fit to the data at all five levels of severity equated the heritabilities and shared environmental influences for males and females, and fixed the DZ[subscript os] coefficient of genetic relatedness at 0.5. Thus, these results provide no evidence for a differential etiology of reading difficulties as a function of gender in more severely impaired samples, and suggest that the same genetic and environmental influences contribute to reading difficulties in males and females, irrespective of severity.

To test the hypothesis that the genetic etiology for reading disability may differ in males and females, data from identical and fraternal twin pairs were analysed using both concordance and multiple regression methods. The sample included 264 identical (129 male, 135 female) and 214 same-sex fraternal (121 male, 93 female) twin pairs in which at least one member of each pair had reading difficulties. The difference between the identical and fraternal twin pair concordance rates was slightly larger for females than for males, suggesting a possible sex difference in etiology; however, a loglinear analysis of the three-way interaction of sex, zygosity, and concordance was not significant (p greater than or equal to 0.17). The estimate of group heritability (h[subscript g][superscript 2]), a standardized measure of the extent to which reading difficulties are due to genetic influences, was somewhat greater for females than males (0.65 vs 0.54), but this difference was also not significant (p greater than or equal to 0.35). Gender differences in h[subscript g][superscript 2] were larger for younger children (less than 11.5 years of age) than for older children. However, the three-way interaction of sex, zygosity, and age was not significant when age was treated either categorically (p greater than or equal to 0.86) or continuously (p greater than or equal to 0.71). Thus, results of this study provide little or no evidence for a differential genetic etiology of reading difficulties in males and females. (Contains 3 tables.)

We report preliminary behaviour genetic analyses of reading and listening comprehension from The Colorado Learning Disabilities Research Center. Although the twin sample with these new measures is still of limited size, we find substantial, and significant, genetic influences on individual differences in both reading and listening comprehension. In addition, word recognition and listening comprehension each accounted for significant "independent" genetic influences on reading comprehension. Together, they accounted for "all" the genetic influence on reading comprehension, indicating a largely genetic basis for the "simple model" of individual differences in reading comprehension proposed by Hoover and Gough (1990).

Prereading and early reading skills of preschool twin children in Australia, Scandinavia and the United States were explored in a genetically sensitive design (max. N=627 preschool pairs and 422 kindergarten pairs). Analyses indicated a strong genetic influence on preschool phonological awareness, rapid naming and verbal memory. Print awareness, vocabulary and grammarmorphology were subject primarily to shared environment effects. There were significant genetic and shared environment correlations among the preschool traits. Kindergarten reading, phonological awareness and rapid naming were primarily affected by genes, and spelling was equally affected by genes and shared environment. Multivariate analyses revealed genetic and environmental overlap and independence among kindergarten variables. Longitudinal analyses showed genetic continuity as well as change in phonological awareness and rapid naming across the 2 years. Relations among the preschool variables of print awareness, phonological awareness and rapid naming and kindergarten reading were also explored in longitudinal analyses. Educational implications are discussed.

Individual differences in measures of prereading skills and in questionnaire measures of 4-5-year-old twins' print environments in Australia, Scandinavia, and the United States were explored with a behavioral-genetic design. Modest phenotypic correlations were found between environmental measures and the twins' print knowledge, general verbal ability, and phoneme awareness. Lower print knowledge in Scandinavian twins was related to country differences in preschool print environment. Latent-trait behavioral-genetic analyses indicated very strong shared-environment influences on individual differences in Print Knowledge. Genetic influence was also significant. Several other prereading skills varied in their environmental and genetic influence, including a significant contrast between Phonological Awareness and Print Knowledge. Rapid Naming also revealed very strong genetic influence, as did Verbal Memory. Stronger shared-environment influences were found for Vocabulary and Grammar/Morphology. Genetic and environmental correlations among latent traits for General Verbal Ability, Phonological Awareness, and Print Knowledge were high, but there were also significant independent genetic and environmental contributions to each skill. Practical implications include the need for substantial and sustained instructional support for children hampered by genetic constraints on early literacy development.

Preliminary results from data on 146 Australian, 284 American, and 70 Norwegian preschool twins indicate reliable genetic influences on phonological awareness and memory and learning. Vocabulary, grammar, and morphology showed significant shared environment and negligible genetic effects. A print knowledge composite showed genetic and shared environment influences. (Contains references.) (Author/CR)

Data from Colorado Adoption Project were used to examine hypothesis that association between parental divorce and children's adjustment is mediated by genetic factors. Findings for psychopathology were consistent with an environmentally mediated explanation for the association. Findings for achievement and social adjustment were consistent with a genetically mediated explanation involving passive genotype-environment correlation. (Author/KB)

Assesses the etiology of the covariation between mathematics performance and general cognitive ability in data from a sample of 555 twins selected for learning deficits and from a sample of 570 control twins pairs. Results show that the phenotypic relationship between mathematics and general cognitive ability is due primarily to genetic influences. (Author/MKA)

To study whether individual differences in general cognitive ability differ in males and females, full-scale IQ data from 426 child twin pairs were fitted to a structural equation model of sex limitation. Individual differences in general cognitive ability appear to be substantially due to common genetic influences in males and females. (SLD)

Comparison of twins (40 identical and 23 fraternal) for mathematics deficits (MD), in which at least one member had a mathematics disability, found evidence for a significant genetic etiology. However, tests for the differential etiology of MD as a function of reading performance level were nonsignificant. (Author/DB)

Data from 148 identical and 111 fraternal twin pairs in which at least 1 member had a reading disability were statistically analyzed. Results suggest that genetic and shared-environment influences both contribute to the observed covariance between reading and mathematical deficits. (Author/DB)

The ε4 allele of APOE is a well-established genetic risk factor for cognitive aging and dementia, but its influence on early life cognition is unknown. Consequently, we assessed associations of APOE genotypes with cognitive performance during 7, 12, and 16 year-assessments in our ongoing Colorado Adoption/Twin Study of Lifespan behavioral development (CATSLife). In general, APOE ε4 was associated with lower Verbal, Performance, and Full Scale IQ scores during childhood and adolescence (e.g., Full Scale IQ was lower by 1.91 points per ε4 allele, d = -0.13), with larger effects in females (e.g., average Full Scale IQ scores were 3.41 points lower in females per each ε4 allele vs. 0.33 points lower in males). Thus, these results suggest that deleterious effects of the APOE ε4 allele are manifested before adulthood, especially in females, and support both early origin theories and differential life-course vulnerabilities for later cognitive impairment.

Because of recent concerns about the replication of published results in the behavioral and biomedical sciences (Ioannidis, PLoS Medicine, Vol. 2, 2005, p. e124; Open Science Collaboration, Science, Vol. 349, 2015, p. 943; Pashler & Wagenmakers, Perspectives on Psychological Science, Vol. 7, 2012, pp. 528–530), we have conducted a replication of our recently published analyses of longitudinal reading performance and attention deficit-hyperactivity disorder data from twin pairs selected for reading difficulties (Wadsworth et al., Twin Research and Human Genetics, Vol. 18, 2015, pp. 755–761). Results obtained from univariate and bivariate (DeFries & Fulker, Behavior Genetics, Vol. 15, 1985, pp. 467–473; Acta Geneticae Medicae et Gemellologiae: Twin Research, Vol. 37, 1988, pp. 205–216) analyses of data from a subset of twin pairs tested in the International Longitudinal Twin Study of Early Reading Development at post-4th grade, and its continuation into high school at post-9th grade, were compared to those from our previous report. Similar measures of reading performance, the same measures of inattention and hyperactivity/impulsivity, and similar selection criteria were used in the two studies. In general, the patterns of results obtained from these two independent studies were highly similar. Thus, these results clearly illustrate the principle that findings from studies in quantitative behavioral genetics often replicate (Plomin et al., Perspectives on Psychological Science, Vol. 11, 2016, pp. 3–23). [ABSTRACT FROM PUBLISHER]

In the context of current concerns about replication in psychological science, we describe 10 findings from behavioral genetic research that have replicated robustly. These are “big” findings, both in terms of effect size and potential impact on psychological science, such as linearly increasing heritability of intelligence from infancy (20%) through adulthood (60%). Four of our top 10 findings involve the environment, discoveries that could have been found only with genetically sensitive research designs. We also consider reasons specific to behavioral genetics that might explain why these findings replicate. [ABSTRACT FROM AUTHOR]

Background Males show higher rates of attention deficit hyperactivity disorder ( ADHD) than do females. Potential explanations include genuine etiological differences or artifact. Methods 2,332 twin and sibling youth participated in behavioral and cognitive testing. Partially competing models of symptom severity distribution differences, the mean difference, and variance difference models, were tested within a randomly selected subsample. The Delta method was used to test for mediation of sex differences in ADHD symptom severity by processing speed, inhibition and working memory. Results The combined mean difference and variance difference models fully explained the sex difference in ADHD symptom severity. Cognitive endophenotypes mediated 14% of the sex difference effect. Conclusions The sex difference in ADHD symptom severity is valid and may be due to differing genetic and cognitive liabilities between the sexes. [ABSTRACT FROM AUTHOR]

We explored the etiology of individual differences in reading development from post-kindergarten to post–4th grade by analyzing data from 487 twin pairs tested in Colorado. Data from three reading measures and one spelling measure were fit to biometric latent growth curve models, allowing us to extend previous behavioral genetic studies of the etiology of early reading development at specific time points. We found primarily genetic influences on individual differences at post–1st grade for all measures. Genetic influences on variance in growth rates were also found, with evidence of small, nonsignificant, shared environmental influences for two measures. We discuss our results, including their implications for educational policy. [ABSTRACT FROM PUBLISHER]

Despite its high heritability, genetic association studies of attention deficit-hyperactivity disorder (ADHD) have often resulted in somewhat small, inconsistent effects. Refining the ADHD phenotype beyond a dichotomous diagnosis and testing associations with continuous information from the underlying symptom dimensions may result in more consistent genetic findings. This study further examined the association between ADHD and the DRD4, DAT1, and 5HTT genes by testing their association with multivariate phenotypes derived from continuous measures of ADHD symptom severity. DNA was collected in 202 families consisting of at least one ADHD proband and at least one parent or sibling. VNTR polymorphisms of the DRD4 and DAT1 genes were significantly associated with the continuous ADHD phenotype. The association with DRD4 was driven by both inattentive and hyperactive symptoms, while the association with DAT1 was driven primarily by inattentive symptoms. These results use novel methods to build upon important connections between dopamine genes and their final behavioral manifestation as symptoms of ADHD. [ABSTRACT FROM AUTHOR]

Although a comparison of concordance rates for deviant scores in identical and fraternal twin pairs can provide prima facie evidence for a genetic etiology, information is not fully utilized when continuous measures are analyzed in a dichotomous manner. Thus, DeFries and Fulker (Behav Genet 15:467–473, ; Acta Genet Med Gemellol, 37:205–216, developed a regression-based methodology (DF analysis) to assess genetic etiology in both selected and unselected twin samples. While the DF analysis is a very versatile and relatively powerful statistical approach, it is not easily extended to the multivariate case. In contrast, structural equation models may be readily extended to analyze multivariate data sets (Neale and Cardon, Methodology for genetic studies of twins and families, ). However, such methodologies may yield biased estimates of additive genetic, shared environmental, and non-shared environmental influences when multivariate models are fitted to selected twin data. Therefore, the Pearson–Aitken (PA) selection formula (Aitken, Proc Edinburgh Math Soc B, 4:106–110, ) was used to analyze reading performance data from twins with reading difficulties (selected sample) and a population of normally-achieving twin pairs (control sample). As a comparison, DF models were also fitted to these same data sets. In general, resulting estimates of additive genetic, shared environmental, and non-shared environmental influences were similar when the DF and PA models were fitted to the data. However, the PA selection formula may be more readily generalized to the multivariate case. [ABSTRACT FROM AUTHOR]

Results obtained from previous longitudinal studies of reading difficulties indicate that reading deficits are generally stable. However, little is known about the etiology of this stability. Thus, the primary objective of this first longitudinal twin study of reading difficulties is to provide an initial assessment of genetic and environmental influences on the stability of reading deficits. Data were analyzed from a sample of 56 twin pairs, 18 identical (monozygotic, MZ) and 38 fraternal (dizygotic, DZ), in which at least one member of each pair was classified as reading-disabled in the Colorado Learning Disabilities Research Center, and on whom follow-up data were available. The twins were tested at two time points (average age of 10.3 years at initial assessment and 16.1 years at follow-up). A composite measure of reading performance (PIAT Reading Recognition, Reading Comprehension and Spelling) was highly stable, with a stability correlation of .84. Data from the initial time point were first subjected to univariate DeFries-Fulker multiple regression analysis and the resulting estimate of the heritability of the group deficit (h2g) was .84 (+/-.26). When the initial and follow-up data were then fitted to a bivariate extension of the basic DF model, bivariate heritability was estimated at .65, indicating that common genetic influences account for approximately 75% of the stability between reading measures at the two time points. [ABSTRACT FROM AUTHOR]

Numerous studies have examined the etiology of the association between reading difficulties and attention-deficit hyperactivity disorder (ADHD) in school-age children, but little is known about the relation between prereading skills and ADHD behaviors prior to the beginning of formal reading instruction. A population-based sample of 809 pairs of preschool twins completed an extensive battery of prereading measures, and the parent of each twin completed an ADHD rating scale. Phenotypic analyses revealed small but significant correlations between DSM-IV inattention ratings and six prereading composite measures, whereas hyperactivity–impulsivity symptoms were not independently associated with any of the prereading scores. Multivariate twin analyses indicated that virtually all of the phenotypic correlation between inattention and prereading performance is attributable to common genetic influences, consistent with results obtained in studies of older twins. Although additional research is needed to test alternative causal models in children younger than five years old, these results are most consistent with the hypothesis that reading difficulties and inattention symptoms are attributable to common genetic influences. [ABSTRACT FROM AUTHOR]

In a test battery consisting of an open-field arena, a light-dark box, a mirror-chamber box, an elevated plus maze, and an elevated square maze, 1,671 mice were tested, generating over 100 putative measures of anxiety in rodents. Quantitative trait loci (QTL) analysis was carried out on all measures, plus composite measures and phenotypic factor scores. Significant LOD scores were found for QTL on 17 chromosomes, with large and consistent QTL behavioral effects on chromosomes 1, 4, 7, 8, 14, 15, l8, and X. QTL on chromosomes 4 and 8 largely influence locomotor activity in both home cages and novel environments, whereas QTL on chromosomes 1, 15, and 18 influence anxiety-related behaviors. Five genetically separable, cross-test dimensions of anxiety could be identified: (i) the suppression of locomotor activity in low to moderately anxiogenic regions of the tests; (ii) a shift toward proportionally less time and activity spent in high-anxiogenic test areas; (iii) the suppression of rearing behavior; (iv) increased latency to enter novel areas; (v) increased autonomic responses, as assessed by defecation and urination. Patterns of QTL influence on cross-test composite scores were distinctive. For example, the QTL on chromosome 1 strongly influenced safe-area locomotor activity (LOD = 35) and autonomic responses (LOD = 16), whereas the QTL on chromosome 15 influenced the proportion of activity in high-anxiogenic areas (LOD = 16), latency to enter novel areas (LOD = 36) and rearing behavior (LOD = 57). Phenotypic factor analysis identified factors heavily loaded on single tests, rather than cross-test factors. The use of factor analysis or within-test principal components for data reduction before genetic analysis was less satisfactory than using genetic dissection methods on the original measures and logically derived composites. [ABSTRACT FROM AUTHOR]

The number and mode of action of quantitative trait loci (QTL) that contribute to behavioral variation in rodents is still largely unknown. On theoretical grounds, multivariate techniques are expected to yield new insights into this problem, but there are only a few examples of its application in practice. Here we explore the power of multivariate approaches to uncover the genetic architecture of 23 anxiety-related phenotypes in 1636 F2 laboratory mice. We detected QTL with a genome-wide significance threshold of P < 0.05 on 14 chromosomes, of which 10 correspond to those identified by univariate analysis. Novel QTL were found on Chromosomes 3, 9, 13, and 17. Thus, multivariate analyses increased the yield of QTL exceeding a genome-wide significance threshold by 40%. On the basis of these results and by the application of a QTL estimator, we show that the mean number of QTL influencing anxiety-related behavior in mice is 6, with a 95% upper limit of 14. [ABSTRACT FROM AUTHOR]

Developmental dyslexia is defined as a specific and significant impairment in reading ability that cannot be explained by deficits in intelligence, learning opportunity, motivation or sensory acuity. It is one of the most frequently diagnosed disorders in childhood, representing a major educational and social problem. It is well established that dyslexia is a significantly heritable trait with a neurobiological basis. The etiological mechanisms remain elusive, however, despite being the focus of intensive multidisciplinary research. All attempts to map quantitative-trait loci (QTLs) influencing dyslexia susceptibility have targeted specific chromosomal regions, so that inferences regarding genetic etiology have been made on the basis of very limited information. Here we present the first two complete QTL-based genome-wide scans for this trait, in large samples of families from the United Kingdom and United States. Using single-point analysis, linkage to marker D18S53 was independently identified as being one of the most significant results of the genome in each scan (P≤0.0004 for single word-reading ability in each family sample). Multipoint analysis gave increased evidence of 18p11.2 linkage for single-word reading, yielding top empirical P values of 0.00001 (UK) and 0.0004 (US). Measures related to phonological and orthographic processing also showed linkage at this locus. We replicated linkage to 18pl 1.2 in a third independent sample of families (from the UK), in which the strongest evidence came from a phoneme-awareness measure (most significant P value=0.00004). A combined analysis of all UK families confirmed that this newly discovered 18p QTL is probably a general risk factor for dyslexia, influencing several readingrelated processes. This is the first report of QTL-based genomewide scanning for a human cognitive trait. [ABSTRACT FROM AUTHOR]

Some evidence exists for the phenotypic association of problem behaviour in early childhood with temperament in infancy, but little is known about the genetic and environmental mechanisms mediating this association. At the ages of 14, 20, 24, and 36 months, mothers of twins completed the Colorado Childhood Temperament Inventory (CCTI; Buss & Plomin, 1984; Rowe & Plomin, 1977). At age 4, problem behaviour was assessed using maternal reports on the Child Behavior Checklist (CBCL/4-18; Achenbach, 1991). The temperamental trait of Emotionality at all four prior age points correlated significantly with the CBCL Total Problem Score at 4 years as well as with the broad-band groupings of Internalising the Externalising. In addition, Shyness at all four ages correlated significantly with the broad-band grouping of Internalising. Longitudinal behavioural genetic analyses indicated that these phenotypic predictions from early temperament to later behaviour problems are largely due to genetic factors. [ABSTRACT FROM AUTHOR]

In order to assess the genetic etiology of the comorbidity of reading and mathematics difficulties, data were ascertained from two samples: (1) 102 identical and 77 same-sex fraternal twin pairs in which at least one member of each pair is reading disabled and (2) 42 identical and 23 same-sex fraternal twin pairs in which at least one member is math disabled. Composite reading and mathematics performance data from each sample were fitted to the basic multiple regression model for the analysis of selected twin data and its bivariate extension. Resulting estimates of bivariate heritability and the genetic correlation between the reading and the mathematics performance measures suggest that the comorbidity between mathematics and reading difficulties is due in part to genetic influences. [ABSTRACT FROM AUTHOR]

Presents a study which examined genetic hypotheses about the mode of transmission of developmental dyslexia by performing complex segregation analyses. Description of the study's design and setting; Possibility of autosomal dominant transmission of dyslexia; Diagnosis of reading disability; Shortcomings of the Colorado Family Reading Study.

Background: Neurocognitive deficits associated with attention-deficit/hyperactivity disorder (ADHD) might be useful intermediate endophenotypes for determining specific genetic pathways that contribute to ADHD. Methods: This study administered 17 measures from prominent neuropsychological theories of ADHD (executive function, processing speed, arousal regulation and, motivation/delay aversion) in dizygotic (DZ) twin pairs discordant for ADHD and control twin pairs (ages 8–18 years) to compare performance between twins affected with ADHD (n = 266), their unaffected co-twins (n = 228), and control children from twin pairs without ADHD or learning difficulties (n = 332). Results: The ADHD subjects show significant impairment on executive function, processing speed, and response variability measures compared with control subjects. Unaffected co-twins of ADHD subjects are significantly impaired on nearly all the same measures as their ADHD siblings, even when subclinical symptoms of ADHD are controlled. Conclusions: Executive function, processing speed, and response variability deficits might be useful endophenotypes for genetic studies of ADHD. [Copyright &y& Elsevier]

Reading performance data from 254 pairs of identical (MZ) and 420 pairs of fraternal (DZ) twins, 8.0 to 20.0 years of age, were subjected to multiple regression analyses. An extension of the DeFries–Fulker (DF) analysis (DeFries & Fulker, 1985, 1988) that facilitated inclusion of data from 303 of their nontwin siblings was employed. In addition to providing estimates of heritability, this analysis yields a test of the difference between shared environmental influences for twins versus siblings (). Results suggest that proband reading deficits are due substantially to genetic factors (.67±.07, p<.001), and that shared environmental influences are significantly higher for members of twin pairs than for those of twins and their nontwin siblings (viz., .25 versus .17, p=.02). [Copyright &y& Elsevier]

Recent psychological and neuropsychological research suggests that executive functions--the cognitive control processes that regulate thought and action--are multifaceted and that different types of executive functions are correlated but separable. The present multivariate twin study of 3 executive functions (inhibiting dominant responses, updating working memory representations, and shifting between task sets), measured as latent variables, examined why people vary in these executive control abilities and why these abilities are correlated but separable from a behavioral genetic perspective. Results indicated that executive functions are correlated because they are influenced by a highly heritable (99%) common factor that goes beyond general intelligence or perceptual speed, and they are separable because of additional genetic influences unique to particular executive functions. This combination of general and specific genetic influences places executive functions among the most heritable psychological traits. These results highlight the potential of genetic approaches for uncovering the biological underpinnings of executive functions and suggest a need for examining multiple types of executive functions to distinguish different levels of genetic influences. [ABSTRACT FROM AUTHOR]

The genetic and environmental contributions to the development of general cognitive ability throughout the first 16 years of life were examined using sibling data from the Colorado Adoption Project. Correlations were analyzed along with structural equation models to characterize the genetic and environmental influences on longitudinal stability and instability. lntraclass correlations reflected both considerable genetic influence at each age and modest shared environmental influence within and across ages. Modeling results suggested that genetic factors mediated phenotypic stability throughout this entire period, whereas most age-to-age instability appeared to be due to nonshared environmental influences. [ABSTRACT FROM AUTHOR]