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By Owen Traubert, Neurobiology; Nageswararao Kanuri, University of Cincinnati; Vincent Fong, Univerity of Cincinnati
Advisor: Shailendra Patel
Awards: Presenter Award: Excellence in Research Communication
Presentation ID: 240
Abstract: Alzheimer's Disease is the 6th leading cause of death in the United States and cannot be cured, prevented, or slowed. A major pathological underpinning of Alzheimer's is buildup of beta-amyloid (Aβ) plaques. Mechanisms affecting Aβ buildup, including its excretion, are therefore an important line of Alzheimer's research, especially in identifying possible targets for treatment. ABCG4 is a transport protein that is present in brain tissue. It has been demonstrated in samples of the blood-brain barrier to effectively transport Aβ and is thought to export it from the brain into the bloodstream. We used a mouse model of Alzheimer's, a mouse line (J9) modified to express the Indiana and Swedish mutations, which cause types of human hereditary Alzheimer's and result in Alzheimer's-like behavior in mice. Some of these mice had ABCG4 production disabled. We tested the hypothesis that loss of the ABCG4 transporter would exacerbate the Alzheimer's-like behavior. We analyzed the following genotypes: ABCG4+/+, J9+ (control), compared to ABCG4-/-, J9+; ABCG4+/-, J9+; and ABCG4-/-, J9- mice with both sexes as separate groups. Three behavioral tests were performed on these groups: open field test (measures anxiety), novel object recognition (measures conceptual memory), and novel object placement (measures spatial memory). We found no significant differences between groups. This indicates that ABCG4 does not play a central role in Alzheimer's, and that if it does have a role, it is redundant. Either its absence can be compensated for by another Aβ-transporting protein, or Aβ transport across the blood-brain barrier is not relevant to Alzheimer's.