Blocked protein stops autism growth in mice

Researchers have successfully blocked a protein in pregnant mice, which may halt the development of foetal autism.

Several studies in the past decade have suggested that changes in a woman’s immune system during pregnancy can lead to the development of autism in her offspring. The changes result in production of the immune signalling protein interleukin-17a (IL-17a), and can result from viral infections, flus and antibiotics.

It is thought that the presence of this protein can double the chance of a foetus developing autism spectrum disorder (ASD).

However, new research led by Gloria B. Choi, from the Massachusetts Institute of Technology in Cambridge, suggests that blocking the immune system-related protein IL-17a in a pregnant mother could stop the foetal onset of ASD.

To mirror the link between the protein and the development of ASD, researchers injected mice with viral infections 12 days into pregnancy, thereby activating their immune systems. This response caused an increase in IL-17a.

By 18 days into gestation the team recorded disrupted neural connections in the cortex of the fetal brain.  Once born, the offspring of the infected mice demonstrated similar traits to those we associate with ASD in humans: slower social development, unusual communication patterns, and repetitive behaviours.

The research team administered another group of pregnant mice with a compound that blocks the production of IL-17a. These mice did not produce IL-17a upon infection, and researchers did not record any disruptions in the foetus’s neural pathways thereafter. Resulting offspring mice did not exhibit behaviours outside the norm.

This finding could hint at possible impacts on human pregnancies and the development of ASD, experts say.

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