Autism spectrum disorders (ASD) are a group of neurodevelopmental conditions characterized by deficits in social communication and repetitive behaviors, which could persist throughout the lifespan. The development of ASD has been associated with many genetic and environmental factors, but the exact biological mechanisms remain unclear. Accelerated biological aging as indicated by shortened telomere length (TL) has been observed in individuals with ASD. Telomeres are nucleoprotein complexes that cap the end of chromosomes to protect DNA from degradation. TL shortens with each round of cell replication and is considered a hallmark of biological aging. Perinatal factors such as parental age at birth have been associated with both ASD risk and TL. While older parental age at birth (mainly father’s age) has been associated with higher ASD risk and longer TL in the offspring, previous research has also found that individuals with ASD had shorter TL than typically developing controls. The contradiction in different aspects of research brings up the parental age-TL-ASD enigma waiting to be resolved through studies looking into their relationships at the same time. This proposed study aims to use the UK biobank cohort to disentangle the complex association between parental age at birth, TL, and ASD in an adult population. Findings from this work will advance TL research under the context of ASD and facilitate early prevention and intervention to promote the health and well-being of individuals at risk of developing ASD. The expected duration of the project is two years from data acquisition to publication.
