Submission Type

Poster

Abstract

Alzheimer’s disease (AD) is one of the most common types of dementia, characterized by progressive memory loss and cognitive decline. Despite its increasing prevalence, there are few treatments and no cure. APOE4 is a variant allele that has been found to contribute to Alzheimer's pathology. We have a knock-in mouse model with the human APOE4 gene that was used to test the cognitive impairment that emerges as a result of the increased APOE4 gene expression. To do this, APOE4 KI mice and wild-type C57BL6/J control mice were tested for activity, motor strength and working memory across development. Although older mice were slower to solve a maze task than younger mice, APOE4 mice were similar to B6 control mice. It may be that an environmental stressor interacts with the APOE4 allele to cause the memory loss characteristic of AD. For example, it is known that the consumption of alcohol exacerbates the onset and magnitude of AD, potentially by increasing neuroinflammation. To test this, we administered EtOH for several days by IP injection. I hypothesized that APOE4 genotype would exacerbate alcohol-induced cognitive impairments.

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Sponsored by Allison Bechard

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059 - The Behavioral Characterization of a Genetic Mouse Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is one of the most common types of dementia, characterized by progressive memory loss and cognitive decline. Despite its increasing prevalence, there are few treatments and no cure. APOE4 is a variant allele that has been found to contribute to Alzheimer's pathology. We have a knock-in mouse model with the human APOE4 gene that was used to test the cognitive impairment that emerges as a result of the increased APOE4 gene expression. To do this, APOE4 KI mice and wild-type C57BL6/J control mice were tested for activity, motor strength and working memory across development. Although older mice were slower to solve a maze task than younger mice, APOE4 mice were similar to B6 control mice. It may be that an environmental stressor interacts with the APOE4 allele to cause the memory loss characteristic of AD. For example, it is known that the consumption of alcohol exacerbates the onset and magnitude of AD, potentially by increasing neuroinflammation. To test this, we administered EtOH for several days by IP injection. I hypothesized that APOE4 genotype would exacerbate alcohol-induced cognitive impairments.

 

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