title: Shortened Telomeres in Families With a Propensity to Autism.
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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Developmental Medicine, Boston Children's Hospital, Harvard Medical School, Boston, and Harvard Graduate School of Education, Cambridge, MA. Electronic address: charles_nelson@harvard.edu.
authors.forename: Charles A
authors.initials: CA
authors.lastname: Nelson
authors.affiliation: Division of Developmental Medicine, Boston Children's Hospital and Harvard Medical School.
authors.forename: Kandice J
authors.initials: KJ
authors.lastname: Varcin
authors.affiliation: Division of Developmental Medicine, Boston Children's Hospital.
authors.forename: Nicole K
authors.initials: NK
authors.lastname: Coman
authors.affiliation: Harvard Medical School, Harvard School of Public Health Program in Genetic Epidemiology, Boston, and Statistical Genetics and Channing Division of Network Medicine, Brigham and Women's Hospital, Boston.
authors.forename: Immaculata
authors.initials: I
authors.lastname: De Vivo
authors.affiliation: Boston University.
authors.forename: Helen
authors.initials: H
authors.lastname: Tager-Flusberg
mesh_terms: D000293:Adolescent; D000328:Adult; D000067877:Autism Spectrum Disorder / Q000235:genetics*; D015415:Biomarkers / Q000032:analysis; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D007223:Infant; D008137:Longitudinal Studies; D008297:Male; D008404:Massachusetts; D008875:Middle Aged; D010290:Parents; D012463:Saliva; D035781:Siblings; D013315:Stress, Psychological; D016615:Telomere / Q000648:ultrastructure*; D055815:Young Adult
chemical_list: D015415:Biomarkers
keywords: autism spectrum disorder; biomarker; psychological stress; telomeres