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Identifying essential cell types and circuits in autism spectrum disorders
Susan E Maloney1, Michael A Rieger, Joseph D Dougherty
1Department of Genetics, Washington University School of Medicine, St. Louis, Missouri, USA; Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri, USA.
International Review of Neurobiology
|December 3, 2013
Summary
Autism spectrum disorder (ASD) has many genetic causes, but may involve a few key cell types. Rodent studies show disrupting specific cells can cause ASD-like behaviors, suggesting multiple pathways to the disorder.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with a strong genetic basis.
- Hundreds of genes are implicated, leading to significant genetic heterogeneity.
- Disruption of specific cell types or neural circuits may underlie ASD, offering therapeutic targets.
Purpose of the Study:
- To review evidence linking specific cell types to ASD etiology.
- To examine rodent models that investigate the sufficiency of cellular disruptions in causing ASD-related behaviors.
- To explore potential convergent cellular pathways in ASD.
Main Methods:
- Review of existing literature on ASD genetics and cellular disruptions.
- Focus on rodent studies examining serotonergic, GABAergic, cerebellar, and striatal cell types.
- Analysis of studies assessing the sufficiency of specific cellular disruptions for ASD-related behaviors.
Main Results:
- Evidence suggests multiple cell types and circuits can contribute to ASD features.
- Disrupting specific cell types (e.g., serotonergic, GABAergic) in rodents can induce ASD-like behaviors.
- The convergence of these cellular disruptions onto a final common circuit remains unclear.
Conclusions:
- Multiple cellular pathways can lead to autism spectrum disorder.
- Understanding these pathways is crucial for developing targeted therapeutic interventions.
- Future research should focus on cellular sufficiency and genetic interactions for patient stratification and treatment development.
