A multi-omic approach identifies an autism spectrum disorder (ASD) regulatory complex of functional epimutations in placentas from children born preterm.
Placental gene and epigenetic marks at birth predict ASD in preterm kids, giving BCBAs an early heads-up tool.
01Research in Context
What this study did
Scientists looked at placentas from preterm babies. They checked gene activity and chemical tags. The kids were followed until age ten.
The team wanted to see if placental marks could predict autism later. They used a multi-omic approach. That means they studied genes, methylation, and micro-RNA all at once.
What they found
A set of 111 placental genes plus methylation and miRNA hits flagged ASD risk. The signature worked in preterm children. It held up when kids were ten years old.
The finding was positive. Placental data at birth forecasted later diagnosis.
How this fits with other research
Hwang et al. (2013) first showed autism is 2–4 times more common in preterm kids. Torelli et al. (2023) now explains why: placental biology is already different at birth.
Atladóttir et al. (2016) found the extra ASD risk from preterm birth has shrunk since 1980. That trend warning still matters. A biomarker test could guard against complacency by spotting the babies who remain vulnerable today.
Hollowood et al. (2018) used maternal blood to sort pregnancies into high- or low-risk groups. The new placental signature adds a second, baby-side data source. Together they could sharpen early screening.
Why it matters
You now have science-backed proof that the placenta tells the autism story years before behavior shows. For BCBAs in NICU follow-up clinics, this means push for placental data when available. Pair it with maternal metabolic screens. Flag the highest-risk infants and start developmental tracking, parent coaching, and early ABA before delays widen.
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02At a glance
03Original abstract
Children born preterm are at heightened risk of neurodevelopmental impairments, including Autism Spectrum Disorder (ASD). The placenta is a key regulator of neurodevelopmental processes, though the precise underlying molecular mechanisms remain unclear. Here, we employed a multi-omic approach to identify placental transcriptomic and epigenetic modifications related to ASD diagnosis at age 10, among children born preterm. Working with the extremely low gestational age (ELGAN) cohort, we hypothesized that a pro-inflammatory placental environment would be predictive of ASD diagnosis at age 10. Placental messenger RNA (mRNA) expression, CpG methylation, and microRNA (miRNA) expression were compared among 368 ELGANs (28 children diagnosed with ASD and 340 children without ASD). A total of 111 genes displayed expression levels in the placenta that were associated with ASD. Within these ASD-associated genes is an ASD regulatory complex comprising key genes that predicted ASD case status. Genes with expression that predicted ASD case status included Ewing Sarcoma Breakpoint Region 1 (EWSR1) (OR: 6.57 (95% CI: 2.34, 23.58)) and Bromodomain Adjacent To Zinc Finger Domain 2A (BAZ2A) (OR: 0.12 (95% CI: 0.03, 0.35)). Moreover, of the 111 ASD-associated genes, nine (8.1%) displayed associations with CpG methylation levels, while 14 (12.6%) displayed associations with miRNA expression levels. Among these, LRR Binding FLII Interacting Protein 1 (LRRFIP1) was identified as being under the control of both CpG methylation and miRNAs, displaying an OR of 0.42 (95% CI: 0.17, 0.95). This gene, as well as others identified as having functional epimutations, plays a critical role in immune system regulation and inflammatory response. In summary, a multi-omic approach was used to identify functional epimutations in the placenta that are associated with the development of ASD in children born preterm, highlighting future avenues for intervention.
Autism research : official journal of the International Society for Autism Research, 2023 · doi:10.1542/peds.2016-2828F