Lack of evidence for genomic instability in autistic children as measured by the cytokinesis-block micronucleus cytome assay.

Autor: Main PA; Sansom Institute of Health Research, University of South Australia, Adelaide, Australia; Department of Animal, Food and Health Sciences, Commonwealth Scientific and Industrial Research Organisation, Adelaide, Australia., Thomas P, Angley MT, Young R, Esterman A, King CE, Fenech MF
Jazyk: angličtina
Zdroj: Autism research : official journal of the International Society for Autism Research [Autism Res] 2015 Feb; Vol. 8 (1), pp. 94-104. Date of Electronic Publication: 2014 Nov 04.
DOI: 10.1002/aur.1428
Abstrakt: 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 (P = 0.027 and P = 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.
(© 2014 International Society for Autism Research, Wiley Periodicals, Inc.)
Databáze: MEDLINE
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