Analysis of Neuroinflammatory Markers in the BTBR T+tf/J Mouse Model of Autism Spectrum Disorder
Location
Ballroom
Start Date
4-5-2018 8:00 AM
End Date
4-5-2018 12:00 PM
Poster Number
84
Name of Project's Faculty Sponsor
Michelle Chandley
Faculty Sponsor's Department
Health Sciences
Type
Poster: Competitive
Project's Category
Biomedical and Health Sciences
Abstract or Artist's Statement
Affecting 1 in 68 children, Autism Spectrum Disorder (ASD) is one of the most prevalent cognitive disorders in the global population. Symptoms of ASD, although typically not life-threatening, have a large impact on the social wellbeing of diagnosed individuals. Inflammation in the brain, or neuroinflammation, has previously been shown to increase the severity of the behavioral deficits associated with ASD. The exact etiology of the neuroinflammation observed in ASD remains unclear, especially in regards to protein expression that initiates the inflammatory pathway. This experiment examines two specific markers of neuroinflammation, glial fibrillary acidic protein (GFAP) and myelin-associated glycoprotein (MAG) in a previously characterized mouse model of ASD. GFAP is astrocyte-specific, cytoplasmic, and has been shown to be upregulated in trauma or disease pathologies in the brain. MAG is found in the membrane of oligodendrocytes and is a major regulator of development and regeneration of nervous tissue. Control C57bl/6j mice and ASD-representative BTBR T+tf/J (BTBR) mice were sacrificed twenty-one days after birth. Immunoblotting was performed on cingulate cortical tissue using anti-GFAP and anti-MAG primary antibodies to quantify levels of GFAP and MAG protein expression between the control and ASD models. These findings provide further evidence that changes in GFAP and MAG expression may alter the neuroinflammatory pathways observed in ASD-representative mice.
Analysis of Neuroinflammatory Markers in the BTBR T+tf/J Mouse Model of Autism Spectrum Disorder
Ballroom
Affecting 1 in 68 children, Autism Spectrum Disorder (ASD) is one of the most prevalent cognitive disorders in the global population. Symptoms of ASD, although typically not life-threatening, have a large impact on the social wellbeing of diagnosed individuals. Inflammation in the brain, or neuroinflammation, has previously been shown to increase the severity of the behavioral deficits associated with ASD. The exact etiology of the neuroinflammation observed in ASD remains unclear, especially in regards to protein expression that initiates the inflammatory pathway. This experiment examines two specific markers of neuroinflammation, glial fibrillary acidic protein (GFAP) and myelin-associated glycoprotein (MAG) in a previously characterized mouse model of ASD. GFAP is astrocyte-specific, cytoplasmic, and has been shown to be upregulated in trauma or disease pathologies in the brain. MAG is found in the membrane of oligodendrocytes and is a major regulator of development and regeneration of nervous tissue. Control C57bl/6j mice and ASD-representative BTBR T+tf/J (BTBR) mice were sacrificed twenty-one days after birth. Immunoblotting was performed on cingulate cortical tissue using anti-GFAP and anti-MAG primary antibodies to quantify levels of GFAP and MAG protein expression between the control and ASD models. These findings provide further evidence that changes in GFAP and MAG expression may alter the neuroinflammatory pathways observed in ASD-representative mice.