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Title: Evaluating the role of social attention in the causal path to Autism Spectrum Disorder
Author: Gui, Anna
ISNI:       0000 0004 8499 5542
Awarding Body: Birkbeck, University of London
Current Institution: Birkbeck (University of London)
Date of Award: 2019
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This thesis evaluated the evidence for the hypothesis that early disruptions in social attention are involved in the causal pathway to Autism Spectrum Disorder (ASD). The sample included infants at high and low familial risk for neurodevelopmental disorders participating in a prospective longitudinal study, and their family members. Five studies were conducted to test whether social attention atypicalities precede the onset of behavioural symptoms and whether they are related to familial, genetic and epigenetic burden for ASD. Chapter 2 examined neural correlates of attention measured with multi-channel electroencephalography in 8-month-old infants attending to faces and non-social stimuli, in relation to outcomes at age 3. Chapter 3 used structural equation modelling to investigate whether disruptions in neural response have cascading effects on learning from the environment via looking behaviour. Next, to further understand whether disruptions in social attention lie between genetic risk and ASD phenotype, Chapter 4 examined the association between ability to detect eye-gaze direction in a familial sample, severity of ASD symptoms and polygenic risk for ASD. Chapter 5 explored these patterns earlier in development, looking at the relationship between social attention at 14 months of age and familial burden, polygenic risk and parentreport traits of ASD and ADHD. Finally, Chapter 6, leveraging DNA methylation data, explored whether epigenetic signals were associated with early neural and behavioural correlates of social attention as well as developmental change leading to atypical outcome. Taken together, this work examined in depth the multifaceted nature of social attention, pointing to neural and behavioural atypicalities at critical time points as promising targets for cognitive and affective interventions. Furthermore, it pioneers future work integrating genetics, epigenetics and early neurocognitive measures of social attention in large prospective longitudinal studies of individuals at increased vulnerability for neurodevelopmental disorders, to shed light on the developmental mechanisms underlying the emergence of ASD.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available