Autism Spectrum Disorders (ASD) are a group of neurodevelopmental disorders characterized by impaired social skills as well as repetitive and restricted behaviors. The prevalence of ASD has increased significantly to 1:54 over the past two decades. Many factors may contribute to ASD development, while the detailed mechanism remains largely unknown. We have previously reported that prenatal exposure to factors such as hormones (e.g., progestin, androgens and estrogens) and maternal diabetes trigger autism-like behaviors (ALB) and gastrointestinal (GI) dysfunction in rodent offspring. In addition, many epidemiological studies showed that prenatal hormone exposure and maternal diabetes are associated with ASD development. Further investigation demonstrated that those prenatal factors trigger epigenetic changes in both progenitor neurons and hematopoietic stem cells, causing persistent gene suppression, and subsequently contributing to ALB in offspring. To be clear, specific gene suppression in peripheral blood mononuclear cells can be a good biomarker for ASD screening, and cord blood stem cell transplantation with related gene manipulation can partly reverse ALB and GI dysfunction in offspring. In this research topic, we are interested in the identification of all potential prenatal risk factors that may contribute to ASD development as well as any potential biomarkers and treatments for either ASD subjects or autism-like phenotype in animal models.
This Research Topic aims to identify any potential prenatal factors that may contribute to ASD development, including but not limited to progestin, maternal diabetes, androgen, estrogen and vitamin D deficiency. Also, it aims to explore possible biomarkers for ASD screening, early postnatal diagnosis and prognosis. Development of potential treatments for autism-like behavior and gastrointestinal dysfunction in animal models or potential clinical treatments for ASD subjects are also encouraged.
In this research topic, we are collecting articles that focus on autism research related to prenatal factor exposures as follows:
• Potential mechanisms for prenatal factor exposure-mediated autism-like behaviors (ALB) and gastrointestinal (GI) dysfunction in both in vitro cells and in vivo animals.
• Development of biological markers for ASD screening, early postnatal diagnosis and prognosis.
• Development of potential treatments for ALB and GI dysfunction in animal models by either prenatal or postnatal through small molecules or stem cells.
• Epidemiological study for ASD-related risk factors and assessment.
• Clinical trials for potential treatments for ASD subjects.
The contributed articles can be Original Research, Reviews, Clinical Trials, and Case Reports.
Autism Spectrum Disorders (ASD) are a group of neurodevelopmental disorders characterized by impaired social skills as well as repetitive and restricted behaviors. The prevalence of ASD has increased significantly to 1:54 over the past two decades. Many factors may contribute to ASD development, while the detailed mechanism remains largely unknown. We have previously reported that prenatal exposure to factors such as hormones (e.g., progestin, androgens and estrogens) and maternal diabetes trigger autism-like behaviors (ALB) and gastrointestinal (GI) dysfunction in rodent offspring. In addition, many epidemiological studies showed that prenatal hormone exposure and maternal diabetes are associated with ASD development. Further investigation demonstrated that those prenatal factors trigger epigenetic changes in both progenitor neurons and hematopoietic stem cells, causing persistent gene suppression, and subsequently contributing to ALB in offspring. To be clear, specific gene suppression in peripheral blood mononuclear cells can be a good biomarker for ASD screening, and cord blood stem cell transplantation with related gene manipulation can partly reverse ALB and GI dysfunction in offspring. In this research topic, we are interested in the identification of all potential prenatal risk factors that may contribute to ASD development as well as any potential biomarkers and treatments for either ASD subjects or autism-like phenotype in animal models.
This Research Topic aims to identify any potential prenatal factors that may contribute to ASD development, including but not limited to progestin, maternal diabetes, androgen, estrogen and vitamin D deficiency. Also, it aims to explore possible biomarkers for ASD screening, early postnatal diagnosis and prognosis. Development of potential treatments for autism-like behavior and gastrointestinal dysfunction in animal models or potential clinical treatments for ASD subjects are also encouraged.
In this research topic, we are collecting articles that focus on autism research related to prenatal factor exposures as follows:
• Potential mechanisms for prenatal factor exposure-mediated autism-like behaviors (ALB) and gastrointestinal (GI) dysfunction in both in vitro cells and in vivo animals.
• Development of biological markers for ASD screening, early postnatal diagnosis and prognosis.
• Development of potential treatments for ALB and GI dysfunction in animal models by either prenatal or postnatal through small molecules or stem cells.
• Epidemiological study for ASD-related risk factors and assessment.
• Clinical trials for potential treatments for ASD subjects.
The contributed articles can be Original Research, Reviews, Clinical Trials, and Case Reports.
