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Deciduous tooth biomarkers reveal atypical fetal inflammatory regulation in autism spectrum disorder
Dani Dumitriu1,2,3, Elena Baldwin2, Roozie J J Coenen2
1Departments of Neuroscience and Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Insights
Prenatal inflammation, measured in baby teeth, may indicate autism spectrum disorder (ASD) risk. Heightened C-reactive protein (CRP) levels in the third trimester of pregnancy were linked to future ASD diagnoses in two independent studies.
Area of Science:
- Neurodevelopmental disorders
- Immunology
- Pediatrics
Background:
- Atypical inflammation is implicated in autism spectrum disorder (ASD) etiology.
- Previous research lacked methods to assess prenatal inflammation's role in ASD development.
- Understanding early inflammatory markers is crucial for identifying developmental risks.
Purpose of the Study:
- To develop a method for profiling prenatal and early childhood inflammation.
- To investigate the association between third-trimester inflammation and later ASD diagnosis.
- To establish a critical developmental window for inflammatory dysregulation in ASD.
Main Methods:
- Utilized archived deciduous teeth to create daily C-reactive protein (CRP) profiles.
- Analyzed CRP levels from the third trimester through early childhood.
- Employed a two-cohort design (Swedish twins and a US study) for discovery and replication.
Main Results:
- Heightened third-trimester CRP levels were observed in children later diagnosed with ASD compared to controls in both discovery and replication cohorts.
- A critical inflammatory window was identified between -90 to -50 days before birth (Swedish cohort) and -128 to -21 days (US cohort).
- The findings demonstrate a consistent association between third-trimester inflammation and ASD risk across different populations.
Conclusions:
- The third trimester represents a critical period for atypical fetal inflammatory regulation in the context of ASD.
- Archived deciduous teeth offer a valuable tool for reconstructing historical inflammatory profiles.
- This research provides novel insights into the prenatal origins of ASD and potential early biomarkers.
Abstract:
Atypical regulation of inflammation has been proposed in the etiology of autism spectrum disorder (ASD); however, measuring the temporal profile of fetal inflammation associated with future ASD diagnosis has not been possible. Here, we present a method to generate approximately daily profiles of prenatal and early childhood inflammation as measured by developmentally archived C-reactive protein (CRP) in incremental layers of deciduous tooth dentin. In our discovery population, a group of Swedish twins, we found heightened inflammation in the third trimester in children with future ASD diagnosis relative to controls (n = 66; 14 ASD cases; critical window: -90 to -50 days before birth). In our replication study, in the US, we observed a similar increase in CRP in ASD cases during the third trimester (n = 47; 23 ASD cases; -128 to -21 days before birth). Our results indicate that the third trimester is a critical period of atypical fetal inflammatory regulation in ASD.
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