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Common EIF4E variants modulate risk for autism spectrum disorders in the high-functioning range.

Regina Waltes¹, Johannes Gfesser, Denise Haslinger

¹Department of Child and Adolescent Psychiatry, Johann Wolfgang Goethe-University, 60528, Frankfurt am Main, Germany.

Journal of Neural Transmission (Vienna, Austria : 1996)

|May 14, 2014

Summary

Common EIF4E gene variants are associated with autism spectrum disorder (ASD) risk and repetitive behaviors. Specific variants show protective or risk effects, suggesting an mRNA pathway in ASD pathogenesis.

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Area of Science:

Genetics
Neuroscience
Psychiatry

Background:

Autism Spectrum Disorders (ASD) have a complex genetic basis, with common variations linked to high-functioning ASD.
Previous research implicated functional variants in EIF4E expression as ASD risk factors.
Modulating EIF4E activity via glutamate receptors reduced repetitive behaviors in human and animal models.

Purpose of the Study:

To investigate the association of common EIF4E variants with overall ASD, strict autism, and the strict high-functioning autism (HFA) subgroup.
To evaluate the effect of these variants on repetitive and/or stereotypic behaviors in ASD cohorts.

Main Methods:

Association analysis of common EIF4E variants (rs13109000, rs4699369, rs12498533) in overall ASD, strict autism, and strict HFA cohorts.
Analysis of the impact of these variants on repetitive and stereotypic behaviors, including hand and finger mannerisms.

Main Results:

Over-transmission of rs13109000G was observed in strict HFA and strict autism cohorts, but not in the overall ASD cohort.
The minor allele of rs4699369T showed a protective effect on stereotyped and ritualized behavior in the overall ASD and strict autism cohorts.
rs4699369T demonstrated a protective role, while rs12498533G showed a risk effect on hand and finger mannerisms.

Conclusions:

Specific EIF4E variants are associated with autism spectrum disorder and repetitive behaviors.
Findings suggest a potential mRNA-mediated pathomechanism for ASD involving EIF4E and its interaction partners.
Replication in larger ASD cohorts is necessary to confirm these genetic associations.