Thursday, May 20, 2010
Franklin Hall B Level 4 (Philadelphia Marriott Downtown)
10:00 AM
S. Lietz
,
MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom
F. Rijsdijk
,
Social, Genetic and Developmental Psychiatry (SGDP) Centre, Institute of Psychiatry, King's College London, London, United Kingdom
E. Colvert
,
MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom
E. Woodhouse
,
MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom
N. Gillan
,
MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom
V. Hallett
,
MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom
P. Bolton
,
MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom
F. Happé
,
MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom
Background: Elevated levels of sensory abnormalities, such as hypo- and hyper-sensitivity to sound, light, touch, and taste, are well-documented in autism (e.g. Leekam et al., 2007, Rogers & Ozonoff, 2005) as well as in Fragile X (Rogers et al., 2003). Since autism and Fragile X are both highly heritable, genetic factors may also be involved in sensory abnormalities. Studies so far indicate moderate heritability of sensory sensitivity in typically developing samples (e.g. Goldsmith et al., 1997), with some indication that the tactile domain might be more heritable than the auditory domain (Goldsmith et al. 2006). A sibling study of sensory abnormalities in ASD (Szatmari et al., 2006) examined the structure of the restricted, repetitive behaviours and interests domain in autism measured by the ADI. Using factor analysis, they found that this domain consists of 2 factors: 'insistence on sameness' (IS) and 'repetitive and sensory motor behaviours and interests' (RSMB). However, their analysis of sibling data did not suggest familiality of the RSMB factor. To date, no twin study of autism has investigated the genetic and environmental contributions to individual differences in sensory responsivity.
Objectives: Using bivariate genetic model-fitting (adjusted to account for selection), this study aims to examine how much of the phenotypic association between sensory abnormalities and autism symptoms is due to genetic and environmental factors shared between each set of symptoms. Furthermore, the relative contribution of genetic and environmental effects to individual differences in sensory responsivity will be estimated.
Methods: This study forms part of a large-scale longitudinal twin study (TEDS - Twins Early Development Study). Twins with ASD (autism, Asperger Syndrome, atypical autism) were recruited for the Social Relationship Study (SRS). The sample for the present study includes 60 ASD twin pairs (at least one twin with ASD) and 60 control twin pairs, aged 12-15 years. Patterns of sensory abnormalities were assessed using the Short Sensory Profile completed by children and parents. The Autism Diagnostic Observation Schedule (ADOS) and Autism Diagnostic Interview-Revised (ADI-R) were carried out to confirm diagnostic status.
Results: Results show moderate phenotypic correlations between total Short Sensory Profile scores and ADI scores. Bivariate Liability Threshold model-fitting analyses will yield the heritability of sensory symptoms and the genetic/environmental correlations between autism symptoms and sensory abnormalities.
Conclusions: Finding genetic overlap between autism and sensory symptoms may indicate that sensory abnormalities are part of the core symptomatology for ASD, and thus could be used as early predictors of ASD as well as being included in diagnostic criteria.
