XVIth European Conference on Developmental Psychology

Lausanne, Switzerland | September 3-7, 2013

UNDERSTANDING ENVIRONMENTAL AND GENETIC INFLUENCES ON NEUROCOGNITIVE DEVELOPMENT

An integrative science symposium co-sponsored by European Association for Developmental Psychology and the Association for Psychological Science

This event occurred on 3 September 2013

Understanding Environmental and Genetic Influences on Neurocognitive Development

Introduction

Annette Karmiloff-Smith, Convenor and Chair, Centre for Brain & Cognitive Development, Birkbeck, University of London

Phenotypes are emergent, not predetermined. From infancy onwards, genetic and environmental vulnerabilities influence gene expression as well as neural, cognitive and behavioural developmental trajectories. The symposium compriseds four talks. The first two will examined how electrophysiology has enhanced our understanding of emerging phenotypes in infants from families with low social economic status and in individuals with autism. The third talk will uncovered how brain imaging and animal models have enriched our knowledge of the development of fear and anxiety in adolescence. The final speaker will discussed how neurocomputational modelling has furthered our understanding of developmental regression in toddlers with autism. The symposium provides an overview of different methods used to uncover the complexities and varieties of emergent phenotypes over developmental time.

Karmiloff-Smith, A., D’Souza, D., Dekker, T. M., Van Herwegen, J., Xu, F., Rodic, M., & Ansari, D. (2012). Genetic and environmental vulnerabilities in children with neurodevelopmental disorders. Proc. Natl. Acad. Sci. USA, 109, 17261-17265.

 

Family Poverty Affects Neural Activity Already in Infancy

Przemek Tomalski, Faculty of Psychology, University of Warsaw, Poland

Family socio-economic status (SES) impacts both structural and functional brain development in childhood, with recent data revealing significant long-term influences on language and attention. Despite the progress in mapping the influence of SES on the developing brain, it remains unknown how early such effects can be demonstrated. This presentation will outline the results of a study of 6-9 month-old infants living in areas of East London with high socio-economic deprivation. Spectral power of resting brain activity in EEG was measured in the awake state. Between-subject comparisons of infants from low- and high-income families revealed significantly lower frontal gamma power in infants from low-income homes. Similar region-specific power differences were found when comparing infants according to maternal occupation, with the infants from lower occupational status groups yielding lower power. These findings will be placed in the context of eye-tracking data from a larger sample of infants with respect to difficulties in processing social and speech cues. Our results indicate that the effects of SES disparities on brain activity and attention to social stimuli can already be detected in early infancy, potentially pointing to very early risk in infancy for subsequent atypical developmental trajectories.

Tomalski, P., Moore, D.G., Ribeiro. H., Axelsson, E., Murphy, E., Karmiloff-Smith, A., Johnson, M.H., & Kushnerenko, E. (in press). Socio-­‐economic status and functional brain development associations in early infancy> Developmenal Science.

 

Electrophysiological Measures in Autism Differentiate Behavioural from Neural Processes

Esha Massand, Centre for Brain & Cognitive Development, Birkbeck, University of London

Recognition memory in ASD (Autism Spectrum Disorder) tends to be comparable to typically developing individuals (Bowler et al., 2000), yet it is unknown whether their memory processes rely on similar or qualitatively different neural mechanisms from the typical case. One way to investigate this is to record online brain electrical activity during item recognition in individuals with ASD compared to age- and IQ-matched healthy controls. Previous event-related potential (ERP) studies on typical individuals have shown that recognition of studied words is accompanied by enhanced positive potentials of words that are correctly identified as ‘old’ from an earlier study phase, compared to words correctly rejected as ‘new’ (old/new ERP effect). The enhanced ERP positivity for old words in typical individuals is assumed to reflect the engagement of cognitive strategies to aid the recognition of an old word (Cycowicz et al., 2001). We used this method to explore neural activity underlying recognition memory in ASD. Behavioural data revealed no overall differences in recognition memory between the ASD and comparison groups. However, ERP data yielded diminished old/new ERP effects in the ASD group, mainly at the central and fronto-central scalp sites. The short-lasting and diminished old/new ERP effect in individuals with ASD indicates that they do not utilise cognitive strategies in a similar manner to typically developing individuals. This study is the first to reveal atypical old/new ERP repetition effects in ASD, and demonstrates that normal recognition behaviour can result from a pattern of differing cognitive and neural processes.

Massand, E., Jemel, B. Mottron, L. & Bowler, D. M. (2013). ERP correlates of recognition memory in autism spectrum disorder. Journal of Autism and Developmental Disorders, Online First.

 

Development of Fear and Anxiety: Human Imaging and Mouse Genetics

BJ Casey, Sackler Institute, Weill Cornell Medical College, New York

Anxiety disorders (e.g., social phobia, separation and generalized anxiety) are the most common of the psychiatric disorders with a lifetime prevalence of nearly 20% and peak in diagnosis during adolescence. One of the most commonly used therapies to treat these disorders is exposure-based cognitive behavioral therapy that relies on basic principles of fear learning and extinction. A substantial portion of patients improves with this therapy, but 40-50% do not. This presentation will provide an overview of our recent empirical studies employing both human imaging and mouse genetics to examine how fear related processes differ across individuals and across development, especially during adolescence. Behavioral, genetic and brain imaging data will be provided to offer insights for whom may be at risk for anxiety and for whom and when, during development, exposure based treatment may be most effective for treating indviduals with anxiety disorders.

Pattwell, S.S., Duhoux, S., Hartley, C.A., Johnson. D.C., Jing, D., Elliott, M.D., Ruberry, E.J., Powers, A., Mehta, N., Yang, R.R., Soliman, F., Glatt, C.E., Casey, B. J.. Ninan, I. & Lee, F.S. (2012). Altered fear learning across development in both mouse and human. PNAS.

 

Regression in Autism: A Neurocomputational Approach

Michael Thomas, Developmental Neurocognition Lab, Birkbeck, University of London

Neurocomputational models are essential tools for investigating the mechanistic causes of developmental deficits. Implemented models force specification of the details of the developmental processes that have gone awry. Models often lead to novel testable predictions. An example is developmental regression which occurs in a subset of young children with autism. It constitutes an apparent reversal of cognitive development in the second year of life, including the loss of previously established skills. The profile of development and loss, as well as the variability in outcome, has proven hard to explain. In this presentation, I use a neurocomputational model to argue that regression in autism is caused by aggressive pruning of brain connections, an exaggeration of a normal phase of brain development that occurs during early childhood. The model has three main virtues. First, it can explain the source of variability observed in the severity and prognosis of regression, by specifying protective and risk factors for the pruning of network connectivity. Second, aggressive pruning may allow us to link the regressive subtype of autism to the broader phenotype; that is, pruning may explain other developmental trajectories of autism, where regression is not observed because the underlying development is slower and/or because the aggressive pruning occurs earlier. Third, the hypothesis generates a number of novel predictions that are both unique and testable via emerging research which is following the development of infants at risk of autism. Most notably, the pruning hypothesis predicts that the earliest symptoms in the emergence of autism should be sensory and motor rather than social, despite a deficit in social skills characterising the adult phenotype.

Thomas, M. S. C., Knowland, V. C. P., & Karmiloff-Smith, A. (2011). Mechanisms of developmental regression in autism and the broader phenotype: A neural network modeling approach. Psychological Review, 118(4), 637-654.

 

General discussion
Annette Karmiloff-Smith, Centre for Brain & Cognitive Development, Birkbeck, University of London