Project Title

Vitamin D receptor gene expression in human and mouse cingulate cortex

Authors' Affiliations

Tiffani Carrasco, Kent Scruggs, Brooke Beasley, Dr. Michelle Chandley, Department of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, TN.

Location

Ballroom

Start Date

4-5-2018 8:00 AM

End Date

4-5-2018 12:00 PM

Poster Number

43

Name of Project's Faculty Sponsor

Michelle Chandley

Faculty Sponsor's Department

Health Sciences

Type

Poster: Competitive

Classification of First Author

Undergraduate Student

Project's Category

Biomedical and Health Sciences

Abstract Text

Autism Spectrum Disorder (ASD) is characterized by a variety of social, sensory, and developmental symptoms. It is estimated that there are 66 cases per 10,000 children in the United States, placing the U.S. in the top ten countries with the highest prevalence of autism. Japan currently has the highest rate at 161 cases per 10,000. There is currently no known cure for this developmental disorder and the diagnostic protocol is not very clear. Those diagnosed are likely to face years of therapy and exposure to different medications to treat the symptoms. However, one risk factor that has received more attention in recent studies is that of Vitamin D and its relationship with ASD. It has been shown that environmental factors can lead to gene expression changes that may affect social behaviors, a core deficit of ASD. Vitamin D deficiencies during development can lead to the upregulation of DNA-repair genes and maternal deficiencies during pregnancy which may inhibit gene repair in the developing fetus. Deficits in Vitamin D have been linked to an increase in the autoimmune response of the body and are thought to lower the immune system’s attack on infections. Quantitative PCR was used to evaluate vitamin D receptor expression in human and mouse homogenate brain tissue punches from the cingulate cortex to determine Vitamin D receptor expression levels. Associations between Vitamin D and ASD may bring us one step closer to determining whether a simple addition of Vitamin D during the prenatal period could help decrease the risk of a developmental disorder such as autism.

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Apr 5th, 8:00 AM Apr 5th, 12:00 PM

Vitamin D receptor gene expression in human and mouse cingulate cortex

Ballroom

Autism Spectrum Disorder (ASD) is characterized by a variety of social, sensory, and developmental symptoms. It is estimated that there are 66 cases per 10,000 children in the United States, placing the U.S. in the top ten countries with the highest prevalence of autism. Japan currently has the highest rate at 161 cases per 10,000. There is currently no known cure for this developmental disorder and the diagnostic protocol is not very clear. Those diagnosed are likely to face years of therapy and exposure to different medications to treat the symptoms. However, one risk factor that has received more attention in recent studies is that of Vitamin D and its relationship with ASD. It has been shown that environmental factors can lead to gene expression changes that may affect social behaviors, a core deficit of ASD. Vitamin D deficiencies during development can lead to the upregulation of DNA-repair genes and maternal deficiencies during pregnancy which may inhibit gene repair in the developing fetus. Deficits in Vitamin D have been linked to an increase in the autoimmune response of the body and are thought to lower the immune system’s attack on infections. Quantitative PCR was used to evaluate vitamin D receptor expression in human and mouse homogenate brain tissue punches from the cingulate cortex to determine Vitamin D receptor expression levels. Associations between Vitamin D and ASD may bring us one step closer to determining whether a simple addition of Vitamin D during the prenatal period could help decrease the risk of a developmental disorder such as autism.