Researchers at Cold Spring Harbor Laboratory report a link between maternal inflammation, placental damage and autism-like traits in male mice. The study suggests that some developmental effects may begin earlier in pregnancy than previously observed, though it does not show that the same process causes autism in people.
The team triggered an immune response in pregnant mice using a substance that mimics the body’s reaction to a viral infection without introducing a virus. Fetuses were especially vulnerable when the response occurred 12.5 days into pregnancy. Around one-third showed developmental abnormalities within 24 hours, according to the researchers.
The effects differed by sex: autism-like traits appeared only in males across the experiments, while females developed normally. The researchers noted that this difference emerged before hormonal surges and other forms of sexual differentiation typically associated with sex-specific development.
When the team examined the placenta, it found damage to specialized cells called spongiotrophoblasts in male fetuses with developmental abnormalities. These cells help the mother’s immune system tolerate the fetus. The researchers suggest that inflammation may disrupt this protective role, potentially allowing the maternal immune response to harm development.
The study raises questions about why female fetuses appeared protected. The researchers propose that females may have a protective mechanism, or that proteins produced by male embryos may prompt a different immune response. They plan to investigate how the responses differ between the sexes.
The findings, published in Science Advances, come from a mouse model and do not establish that placental damage or maternal inflammation causes autism in humans. The researchers say the work may help identify biological pathways involved in early development and guide further study of possible intervention targets.
Sources: ScienceDaily.