Time to give up on a single explanation for autism

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Abstract

We argue that there will be no single (genetic or cognitive) cause for the diverse symptoms defining autism. We present recent evidence of behavioral fractionation of social impairment, communication difficulties and rigid and repetitive behaviors. Twin data suggest largely nonoverlapping genes acting on each of these traits. At the cognitive level, too, attempts at a single explanation for the symptoms of autism have failed. Implications for research and treatment are discussed.

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Most cited references 22

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Executive dysfunction in autism☆

Elisabeth Hill (2004)

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Broader autism phenotype: evidence from a family history study of multiple-incidence autism families.

J. Piven, P. Palmer, D Jacobi … (1997)

Studies of families ascertained through a single autistic proband suggest that the genetic liability for autism may be expressed in nonautistic relatives in a phenotype that is milder but qualitatively similar to the defining features of autism. The objective of this study was to examine behaviors that may define this broader phenotype in relatives ascertained through two autistic siblings. The authors used a semistructured family history interview to compare the rates of social and communication deficits and stereotyped behaviors in relatives ascertained through two autistic siblings (families with multiple-incidence autism; 25 families) with the rates in relatives of Down syndrome probands (30 families). Higher rates of social and communication deficits and stereotyped behaviors were found in the relatives in the families with multiple-incidence autism. These data suggest that further studies should be undertaken to delineate the boundaries of the broader autism phenotype and that this broader phenotype should be included in some future genetic analyses of this disorder.

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Genetic heterogeneity between the three components of the autism spectrum: a twin study.

Angelica Ronald, Francesca Happé, Patrick Bolton … (2006)

This study investigated the etiology of autistic-like traits in the general population and the etiological overlap between the three aspects of the triad of impairments (social impairments, communication impairments, restricted repetitive behaviors and interests) that together define autism spectrum disorders. Parents of 3,400 8-year-old twin pairs from the Twins Early Development Study completed the Childhood Asperger Syndrome Test, a screening instrument for autism spectrum symptoms in mainstream samples. Genetic model-fitting of categorical and continuous data is reported. High heritability was found for extreme autistic-like traits (0.64-0.92 for various cutoffs) and autistic-like traits as measured on a continuum (0.78-0.81), with no significant shared environmental influences. All three subscales were highly heritable but showed low covariation. In the genetic modeling, distinct genetic influences were identified for the three components. These results suggest the triad of impairments that define autism spectrum disorders is heterogeneous genetically. Molecular genetic research examining the three components separately may identify different causal pathways for the three components. The analyses give no indication that different genetic processes affect extreme autistic impairments and autistic impairments as measured on a continuum, but this can only be directly tested once genes are identified.