Associations Between Genetic Risk for Alzheimer's Disease and Hippocampus-Dependent Memory and Learning in Healthy, Middle-Aged Adults
Mentor 1
Ira Driscoll
Location
Union Wisconsin Room
Start Date
28-4-2017 1:30 PM
End Date
28-4-2017 4:00 PM
Description
Both normal and pathological aging are accompanied by memory decline. The epsilon 4 (e4) allele of the apolipoprotein E (APOE) gene is the best-established genetic risk factor for Alzheimer's disease (AD) which is behaviorally hallmarked by memory loss. We focused our considerations on the hippocampus based on the fact that (1) the hippocampus is critically involved in memory, and (2) is especially vulnerable to the deleterious effects of aging. We employed the virtual Morris water task (vMWT) to assess hippocampus-dependent spatial learning and memory. The vMWT is a translational version of the classic paradigm used to investigate place learning and memory in rodents and requires participants to acquire, consolidate, and retrieve distal spatial cues to navigate a large pool and find a hidden escape-platform. The objective of the present study was to assess the association between the APOE gene and spatial learning and memory using the vMWT. We hypothesized that APOE e4 risk-carriers would have longer latencies and travel longer distances to find the platform during learning trials. Furthermore, we predicted that the APOE4 risk-carriers would have lower latency and travel shorter distance in the goal quadrant of the vMWT probe trial, all indicators of poor learning and memory. In our sample of healthy, middle-aged adults (N=143; age 40-61), APOE e4 risk-carriers traveled significantly shorter distance in the goal quadrant of the probe trial, and there was a trend toward higher total latency in finding a hidden platform across the learning trials. These outcomes signify poorer spatial learning and memory in the APOE e4 risk-carriers, when compared to the non-carriers. Our findings indicate that the vMWT may be a useful early detector of cognitive changes, and that memory deficits may be present early and well prior to any clinical impairment in those at genetic risk for AD.
Associations Between Genetic Risk for Alzheimer's Disease and Hippocampus-Dependent Memory and Learning in Healthy, Middle-Aged Adults
Union Wisconsin Room
Both normal and pathological aging are accompanied by memory decline. The epsilon 4 (e4) allele of the apolipoprotein E (APOE) gene is the best-established genetic risk factor for Alzheimer's disease (AD) which is behaviorally hallmarked by memory loss. We focused our considerations on the hippocampus based on the fact that (1) the hippocampus is critically involved in memory, and (2) is especially vulnerable to the deleterious effects of aging. We employed the virtual Morris water task (vMWT) to assess hippocampus-dependent spatial learning and memory. The vMWT is a translational version of the classic paradigm used to investigate place learning and memory in rodents and requires participants to acquire, consolidate, and retrieve distal spatial cues to navigate a large pool and find a hidden escape-platform. The objective of the present study was to assess the association between the APOE gene and spatial learning and memory using the vMWT. We hypothesized that APOE e4 risk-carriers would have longer latencies and travel longer distances to find the platform during learning trials. Furthermore, we predicted that the APOE4 risk-carriers would have lower latency and travel shorter distance in the goal quadrant of the vMWT probe trial, all indicators of poor learning and memory. In our sample of healthy, middle-aged adults (N=143; age 40-61), APOE e4 risk-carriers traveled significantly shorter distance in the goal quadrant of the probe trial, and there was a trend toward higher total latency in finding a hidden platform across the learning trials. These outcomes signify poorer spatial learning and memory in the APOE e4 risk-carriers, when compared to the non-carriers. Our findings indicate that the vMWT may be a useful early detector of cognitive changes, and that memory deficits may be present early and well prior to any clinical impairment in those at genetic risk for AD.
