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Spectrum: Autism Research News

Genetic influence over social skills shifts as children grow

by  /  14 December 2017
four teenage friends sitting outside in parking lot
Puberty plummet: The genetic influence on social communication, as measured by scores on an autism checklist, dips at age 14 but rises again at 17.

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This article is more than five years old. Autism research — and science in general — is constantly evolving, so older articles may contain information or theories that have been reevaluated since their original publication date.

The combinations of genetic variants that influence social communication vary throughout childhood and adolescence, a new study suggests1.

Researchers used an algorithm to track the evolution of this genetic association with social communication in the same group of children over 10 years. They found that the influence of one set of genetic factors waxes and wanes from ages 11 to 17.

The approach provides a way to tease apart the genetic factors that govern social communication and other complex traits during different stages of development, the researchers say.

The study “clearly shows that we have to take development into account when we look at behavior,” says lead investigator Beate St Pourcain, researcher at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands. “It’s natural that our social behavior changes during the course of development — and of course the genetic causes will change with it.”

The developmental pattern in genetic influence the researchers observed “[suggests] that the genetic influences on social development that come into play after puberty, although they can also cause communication difficulties, are different than those predisposing to autism,” says David Skuse, professor of behavioral and brain sciences at University College London. (Skuse was not involved in the work but has collaborated with St Pourcain previously.)

And “it suggests that there are genetic influences operating that are somewhat different during different stages of development,” says Skuse.

Teen trends:

In a study published in January, St Pourcain and her colleagues reported that the combinations of genetic factors that govern social skills in teenagers with autism or schizophrenia differ from those in typical teenagers2.

In that study, the researchers looked at behavioral and genetic data from the Avon Longitudinal Study of Parents and Children — which tracks health and development in more than 5,000 typically developing children — and databases of people with autism or schizophrenia.

They found that the genetic factors governing social communication problems in autism strongly correlate with those in typical children when the children are young. But this overlap decreases in adolescence. For schizophrenia, they found the reverse pattern: The overlap is weak in early childhood and strongest at 17 years of age.

These observations hinted that a new genetic factor contributing to social communication may emerge in adolescence.

In the new work, the researchers explored this hypothesis directly using data from 5,551 children in the Avon cohort. The children were assessed for social communication difficulties at ages 8, 11, 14 and 17 using the Social Communication Disorder Checklist (SCDC).

Previous research had shown that a significant component of the variation in SCDC scores is attributable to genetic factors3. So the researchers looked at whether the factors linked to SCDC scores at one age remain associated with them at later ages.

They found that the set of genetic variants associated with SCDC scores at age 8 is also present at the later ages. However, at age 11, another set of genetic variants comes into play. At age 14, the influence that these two sets have on the scores plummets. But by age 17, the sway of the early-childhood set re-emerges, and the influence of the second set grows to an equal level of importance. The findings were published in September in Biological Psychiatry.

As this trajectory plays out, it is accompanied by changes in social behavior, such as increased empathy and self-control, as well as changes in the brain, such as the pruning of neuronal connections, St Pourcain says.

Other autism traits, such as repetitive behaviors, may not show this trend in genetic influence, she says.

Plastic period:

The new results mirror findings in Skuse’s lab showing that girls and boys both become worse at interpreting facial expressions in adolescence.

“It points a finger at something going on around the time of puberty that involves the reorganization of genetic influences on our social communication competence,” Skuse says.

The findings might even hint that puberty is an especially good time to try to treat a neurodevelopmental condition such as autism, he says. “I’m speculating wildly, but it does suggest that the brain becomes more plastic during that time.”

The work is in typical children, so researchers first need to confirm that the findings hold in children with the condition, says John Constantino, co-director of the Intellectual and Developmental Disabilities Research Center at Washington University in St Louis, who was not involved in the study.

The work is “a provocative analysis from a very experienced team,” Constantino says. But only one-third or less of the variance in SCDC scores has a genetic basis, he notes. By contrast, autism overall “is very strongly influenced by genetic factors and extremely stable over time.”

The set of genetic variants identified in adolescence may also not contribute to autism because the condition’s roots lie in early development. The Avon study did not collect SCDC scores for children before age 8, so investigating earlier ages would require additional data, says St Pourcain.

Her team is exploring the genetic influence on other behavioral traits associated with autism, such as behavior problems and hyperactivity.

Corrections

This story has been changed to indicate that genetic factors account for a significant component of variation in the SCDC scores, rather than the scores themselves.


References:
  1. St Pourcain B. et al. Biol. Psychiatry Epub ahead of print (2017) PubMed
  2. St Pourcain B. et al. Mol. Psychiatry Epub ahead of print (2017) PubMed
  3. St Pourcain B. et al. Mol. Autism 5, 18 (2014) PubMed
TAGS:   autism