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Published on: October 3, 2018
Reduced face identity aftereffects in relatives of children with autism
Chiara Fiorentini1, Laura Gray2, Gillian Rhodes3
1Institute of Child Health, University College London, London; Department of Psychology, The Australian National University, Australia; ARC Centre of Excellence in Cognition and its Disorders, School of Psychology, University of Western Australia, Australia.
Abstract:
Autism is a pervasive developmental condition with complex aetiology. To aid the discovery of genetic mechanisms, researchers have turned towards identifying potential endophenotypes - subtle neurobiological or neurocognitive traits present in individuals with autism and their "unaffected" relatives. Previous research has shown that relatives of individuals with autism exhibit face processing atypicalities, which are similar in nature albeit of lesser degree, to those found in children and adults with autism. Yet very few studies have examined the underlying mechanisms responsible for such atypicalities. Here, we investigated whether atypicalities in adaptive norm-based coding of faces are present in relatives of children with autism, similar to those previously reported in children with autism. To test this possibility, we administered a face identity aftereffect task in which adaptation to a particular face biases perception towards the opposite identity, so that a previously neutral face (i.e., the average face) takes on the computationally opposite identity. Parents and siblings of individuals with autism showed smaller aftereffects compared to parents and siblings of typically developing children, especially so when the adapting stimuli were located further away from the average face. In addition, both groups showed stronger aftereffects for adaptors far from the average than for adaptors closer to the average. These results suggest that, in relatives of children with autism, face-coding mechanism are similar (i.e., norm-based) but less efficient than in relatives of typical children. This finding points towards the possibility that diminished adaptive mechanisms might represent a neurocognitive endophenotype for autism.
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