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Attention is construed as multicomponential, but the roles of its distinct subfunctions in shaping the broader developing cognitive landscape are poorly understood. The current study assessed 3- to 6-year-olds (N = 83) to: (a) trace developmental trajectories of attentional processes and their structure in early childhood and (b) measure the impact of distinct attention subfunctions on concurrent and longitudinal abilities related to literacy and numeracy. Distinct trajectories across attention measures revealed the emergence of 2 attentional factors, encompassing \"executive\" and \"sustained—selective\" processes. Executive attention predicted concurrent abilities across domains at Time 1, whereas sustained—selective attention predicted basic numeracy 1 year later. These concurrent and longitudinal constraints cast a broader light on the unfolding relations between domain-general and domain-specific processes over early childhood.

Individuals with Down syndrome have an enhanced risk of developing early onset Alzheimer disease. Here, the authors describe the features of Alzheimer disease in Down syndrome and show how understanding the genetic and pathogenic mechanisms of this form of Alzheimer disease may shed light on more general mechanisms of neurodegeneration. Down syndrome, which arises in individuals carrying an extra copy of chromosome 21, is associated with a greatly increased risk of early-onset Alzheimer disease. It is thought that this risk is conferred by the presence of three copies of the gene encoding amyloid precursor protein (APP) — an Alzheimer disease risk factor — although the possession of extra copies of other chromosome 21 genes may also play a part. Further study of the mechanisms underlying the development of Alzheimer disease in people with Down syndrome could provide insights into the mechanisms that cause dementia in the general population.

Dagmara Annaz University College London Daniel Ansari University of Western Ontario, Canada Gaia Scerif University of Oxford, United Kingdom Chris Jarrold University of Bristol, United Kingdom Annette Karmiloff-Smith Birkbeck College Contact author: Michael Thomas, Developmental Neurocognition Laboratoy, School of Psychology, Birkbeck College, University of London, Malet Street, Bloomsbury, London WC1E 7HX, United Kingdom. E-mail: m.thomas{at}bbk.ac.uk . Purpose: In this article, the authors present a tutorial on the use of developmental trajectories for studying language and cognitive impairments in developmental disorders and compare this method with the use of matching. Method: The authors assess the strengths, limitations, and practical implications of each method. The contrast between the methodologies is highlighted using the example of developmental delay and the criteria used to distinguish delay from atypical development. Results: The authors argue for the utility of the trajectory approach, using illustrations from studies investigating language and cognitive impairments in individuals with Williams syndrome, Down syndrome, and autism spectrum disorder. Conclusion: Two conclusions were reached: (a) An understanding of the underlying mechanism will be furthered by the richer descriptive vocabulary provided by the trajectories approach (e.g., in distinguishing different types of delay) and (b) an optimal design for studying developmental disorders is to combine initial cross-sectional designs with longitudinal follow-up. KEY WORDS: development, trajectories, delay, deviance, disorders CiteULike     Connotea     Del.icio.us     Digg     Facebook     Reddit     Technorati     Twitter     What's this?

Much progress has been made toward behavioral and pharmacological intervention in intellectual disability, which was once thought too difficult to treat. Down syndrome (DS) research has shown rapid advances, and clinical trials are currently underway, with more on the horizon. Here, we review the literature on the emergent profile of cognitive development in DS, emphasizing that treatment approaches must consider how some \"end state\" impairments, such as language deficits, may develop from early alterations in neural systems beginning in infancy. Specifically, we highlight evidence suggesting that there are pre- and early postnatal alterations in brain structure and function in DS, resulting in disturbed network function across development. We stress that these early alterations are likely amplified by Alzheimer's disease (AD) progression and poor sleep. Focusing on three network hubs (prefrontal cortex, hippocampus, and cerebellum), we discuss how these regions may relate to evolving deficits in cognitive function in individuals with DS, and to their language profile in particular.

One might expect that children with varying genetic mutations or children raised in low socioeconomic status environments would display different deficits. Although this expectation may hold for phenotypic outcomes in older children and adults, cross-syndrome comparisons in infancy reveal many common neural and sociocognitive deficits. The challenge is to track dynamic trajectories over developmental time rather than focus on end states like in adult neuropsychological studies. We contrast the developmental and adult approaches with examples from the cognitive and social domains, and we conclude that static models of adult brain lesions cannot be used to account for the dynamics of change in genetic and environmentally induced disorders in children.

Background Down syndrome (DS) is associated with variable intellectual disability and multiple health and psychiatric comorbidities. The impact of such comorbidities on cognitive outcomes is unknown. We aimed to describe patterns of physical health and psychiatric comorbidity prevalence, and receptive language ability, in DS across the lifespan, and determine relationships with cognitive outcomes. Methods Detailed medical histories were collected and cognitive abilities measured using standardised tests for 602 individuals with DS from England and Wales (age range 3 months to 73 years). Differences in prevalence rates between age groups and between males and females were determined using chi-squared or Fisher’s exact tests. In adults, rates for psychiatric comorbidities were compared to expected population rates using standardised morbidity ratios (SMRs). Adapted ANCOVA functions were constructed to explore age and sex associations with receptive language ability across the lifespan, and regression analyses were performed to determine whether the presence of health comorbidities or physical phenotypes predicted cognitive abilities. Results Multiple comorbidities showed prevalence differences across the lifespan, though there were few sex differences. In adults, SMRs were increased in males and decreased in females with DS for schizophrenia, bipolar disorder, and anxiety. Further, SMRs were increased in both males and females with DS for dementia, autism, ADHD, and depression, with differences more pronounced in females for dementia and autism, and in males for depression. Across the lifespan, receptive language abilities increasingly deviated from age-typical levels, and males scored poorer than females. Only autism and epilepsy were associated with poorer cognitive ability in those aged 16–35 years, with no relationships for physical health comorbidities, including congenital heart defects. Conclusions Our results indicate the prevalence of multiple comorbidities varies across the lifespan in DS, and in adults, rates for psychiatric comorbidities show different patterns for males and females relative to expected population rates. Further, most health comorbidities are not associated with poorer cognitive outcomes in DS, apart from autism and epilepsy. It is essential for clinicians to consider such differences to provide appropriate care and treatment for those with DS and to provide prognostic information relating to cognitive outcomes in those with comorbidities.

In this article, we first present a summary of the general assumptions about Down syndrome (DS) still to be found in the literature. We go on to show how new research has modified these assumptions, pointing to a wide range of individual differences at every level of description. We argue that, in the context of significant increases in DS life expectancy, a focus on individual differences in trisomy 21 at all levels-genetic, cellular, neural, cognitive, behavioral, and environmental-constitutes one of the best approaches for understanding genotype/phenotype relations in DS and for exploring risk and protective factors for Alzheimer's disease in this high-risk population.

In typical infants, the achievement of independent locomotion has a positive impact on the development of both small-scale and large-scale spatial cognition. Here we investigated whether this association between the motor and spatial domain: (1) persists into childhood and (2) is detrimental to the development of spatial cognition in individuals with motor deficits, namely, individuals with attention deficit hyperactivity disorder (ADHD) and individuals with Williams syndrome (WS). Despite evidence of a co-occurring motor impairment in many individuals with ADHD, little is known about the developmental consequences of this impairment. Individuals with WS demonstrate impaired motor and spatial competence, yet the relationship between these two impairments is unknown. Typically developing (TD) children ( = 71), individuals with ADHD ( = 51), and individuals with WS ( = 20) completed a battery of motor tasks, a measure of independent exploration, and a virtual reality spatial navigation task. Retrospective motor milestone data were collected for the ADHD and WS groups. Results demonstrated a relationship between fine motor ability and spatial navigation in the TD group, which could reflect the developmental impact of the ability to manually manipulate objects, on spatial knowledge. In contrast, no relationships between the motor and spatial domains were observed for the ADHD or WS groups. Indeed, while there was evidence of motor impairment in both groups, only the WS group demonstrated an impairment in large-scale spatial navigation. The motor-spatial relationship in the TD, but not the ADHD and WS groups, suggests that aspects of spatial cognition can develop via a developmental pathway which bypasses input from the motor domain.

The ability to reproduce novel words is a sensitive marker of language impairment across a variety of developmental disorders. Nonword repetition tasks are thought to reflect phonological short-term memory skills. Yet, when children hear and then utter a word for the first time, they must transform a novel speech signal into a series of coordinated, precisely timed oral movements. Little is known about how children's oromotor speed, planning and co-ordination abilities might influence their ability to repeat novel nonwords, beyond the influence of higher-level cognitive and linguistic skills. In the present study, we tested 35 typically developing children between the ages of 5-8 years on measures of nonword repetition, digit span, memory for non-verbal sequences, reading fluency, oromotor praxis, and oral diadochokinesis. We found that oromotor praxis uniquely predicted nonword repetition ability in school-age children, and that the variance it accounted for was additional to that of digit span, memory for non-verbal sequences, articulatory rate (measured by oral diadochokinesis) as well as reading fluency. We conclude that the ability to compute and execute novel sensorimotor transformations affects the production of novel words. These results have important implications for understanding motor/language relations in neurodevelopmental disorders.

There is evidence that sleep enhances memory and learning. Childhood is a critical period for neurodevelopment, and minor but persistent disruption of sleep may have long-term implications for cognitive performance. Sleep is critical for health and is undervalued both in our 24 h society and in paediatric clinical practice. Paediatricians need to understand the neurodevelopmental consequences of poor quality sleep in children.