Shortened Telomeres in Families With a Propensity to Autism - 16/06/15
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Abstract |
Objective |
Shortened telomeres have been linked to poorer health outcomes. Exposure to psychological stress is associated with accelerated telomere shortening, and a well-established body of evidence indicates that families with a child with autism spectrum disorder (ASD) experience heightened levels of psychological stress. Also, alterations in a number of biological processes implicated in telomere length dynamics (i.e., oxidative stress, DNA methylation) have been linked to ASD susceptibility. We examined whether families of children with ASD who have an infant show shortened telomeres.
Method |
Saliva samples were collected from infants, their older sibling (proband), and parents in families with or without a child with ASD. Infants and their families were designated as high-risk for ASD (HRA; n = 86) or low-risk for ASD (LRA; n = 118) according to the older siblings’ diagnostic status. We used the real-time polymerase chain reaction (PCR) telomere assay to determine relative average telomere length for each participant.
Results |
HRA families demonstrated significantly shorter telomere length relative to LRA families. This effect was observed at the individual family member level, with infants, probands, and mothers in HRA families showing reduced relative telomere length compared to individuals in LRA families; although not significant, fathers of high-risk infants showed a similar pattern of decreased telomere length.
Conclusion |
Families of children with ASD who have an infant show shortened telomeres relative to families with no history of ASD. These results suggest that such “high-risk” families should be monitored for the physical and mental health consequences that are often associated with accelerated telomere shortening.
Le texte complet de cet article est disponible en PDF.Key Words : autism spectrum disorder, telomeres, biomarker, psychological stress
Plan
This article is discussed in an editorial by Dr. Stacy S. Drury on page 539. |
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Support for this work was provided by the National Institutes of Health (NIH; 1R01DC010290 to H.T.-F. and C.A.N.), the Simons Foundation (grant# 137186 to C.A.N.), the Philanthropic Council of the Division of Developmental Medicine, Boston Children’s Hospital (to C.A.N.), an anonymous foundation (to C.A.N.), and the NIH to De Vivo (R01 CA082838 and PO1CA006516). |
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Disclosure: Drs. Nelson, Varcin, DeVivo, Tager-Flusberg, and Ms. Coman report no biomedical financial interests or potential conflicts of interest. |
Vol 54 - N° 7
P. 588-594 - juillet 2015 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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