Lack of Evidence for Genomic Instability in Autistic Children as Measured by the Cytokinesis‐Block Micronucleus Cytome Assay. Issue 1 (4th November 2014)

• Record Type: Journal Article
• Authors: Main, Penelope A.E.; Thomas, Philip; Angley, Manya T.; Young, Robyn; Esterman, Adrian; King, Catherine E.; Fenech, Michael F.
• Is Part Of: Autism research. Volume 8:Issue 1(2015:Feb.)
• Page Start: 94
• Page End: 104
• Publication Date: 2014-11-04
• Subjects: Autism -- Periodicals; Autism -- Research -- Periodicals; 616.85882005
• DOI: 10.1002/aur.1428
• Languages: English
• ISSNs: 1939-3792

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Autism spectrum disorders are a set of neurodevelopmental disorders that are highly hereditable. Increased genomic instability has been observed in other heritable paediatric neurobiological disorders; therefore, the aim of our study was to test the hypothesis that DNA damage is increased in children with autism and that B vitamin status may explain variations in genome integrity between autistic and normal children. We compared 35 children with autism, 27 of their siblings without autism and 25 age‐ and gender‐matched community controls for genomic stability using the cytokinesis‐block micronucleus cytome (CBMN‐cyt) assay, B vitamins and homocysteine, as well as autism‐related behaviours. It was found that there were no differences in CBMN‐cyt biomarkers between the three groups. Vitamin B2 was significantly raised in children with autism and their siblings compared with controls (<italic>P</italic> = 0.027 and <italic>P</italic> = 0.016 respectively) but there was no difference in other B vitamins or homocysteine. In conclusion, although replication using a larger cohort is needed, it appears unlikely that genomic instability is a feature of the aetiology of autism. We cannot rule out in utero effects or other types of DNA damage not measured by the CBMN‐cyt assay. <bold><italic>Autism Res</italic></bold><italic>2015, 8: 94–104</italic>. © 2014 International Society for Autism Research, Wiley Periodicals, Inc.</p> </abstract>