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Role of Infection and Immune Activation During Pregnancy in the Etiology of Autism

Friday, 3 May 2013: 12:30
Auditorium (Kursaal Centre)
H. O. Atladottir, University of Aarhus, Aarhus, Denmark
Background: An increasing number of scientific papers have suggested that maternal infection and maternal immune activation during pregnancy are associated with the development of autism. The literature in the field has increased extensively during the last decade and includes case reports, studies on inflammatory markers in humans, animal experimental studies, and epidemiological studies.

Objectives: The main purpose of this presentation is to give a brief overview of the scientific literature concerning infection and maternal immune activation and the development of autism. Potential mechanisms on how maternal infection and maternal immune activation can be etiologically associated to the development of autism will be described. Findings from epidemiological studies will be discussed in the light of results from case reports and animal studies.  

Methods: The presentation includes a systematic walk-through of important scientific findings published during the last decade concerning infections and immune activation during pregnancy and development of autism. The audience will get an overall view of the literature with focus on consistency in findings. The strengths and limitations of especially epidemiological research will be discussed as well as the importance of cautious interpretation of results from epidemiological studies.  

Results: Early case reports and comparative studies have suggested maternal prenatal viral infections to be associated with the development of ASD.  Results from recent animal studies suggest that infection-induced maternal immune activation leads to a fetal inflammatory response that has been implicated in the development of autism. However, the picture is still incomplete, and data mostly experimental. Only few epidemiological studies have investigated the association between specific infectious diseases in pregnancy and development of autism. These epidemiological studies have had methodological limitations, such as limited completeness and validity of exposure data. While not definitive, the findings have been suggestive of a link.  

Conclusions: Infection and immune activation during pregnancy is possibly an important etiological factor in the development of autism in certain individuals. Future research will most likely continue to focus on how specific immunological reactions during pregnancy are associated with autism, and with time research will presumably focus more on the interaction between genetics and immune system insults. Future epidemiological studies can benefit from validated data on infectious exposure. Whenever possible, scientists doing autism research should consider including other neurodevelopmental outcomes in order to explore the autism specificity of their results.

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