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Memory function in a mouse genetic model of Alzheimer's disease
Avdesh Avdesh1, Patrick Wong, Ralph N Martins
1Centre of Excellence for Alzheimer's Disease Research and Care, Edith Cowan University, Perth, WA, Australia.
Journal of Alzheimer'S Disease : JAD
|April 5, 2011
Summary
Apolipoprotein E4 (ApoE4) gene variants increase Alzheimer's risk. ApoE knockout mice showed improved spatial memory, but combination antioxidant therapy had no effect on cognitive deficits.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- The apolipoprotein E (ApoE) E4 allele is a significant risk factor for late-onset Alzheimer's disease (AD).
- ApoE knockout (ApoE KO) mice exhibit AD pathologies like neurofibrillary tangles and senile plaques, but cognitive deficits remain inconclusive.
- Existing memory models, such as the Morris water maze, may not fully capture cognitive impairments in ApoE KO mice.
Purpose of the Study:
- To investigate spatial memory in ApoE KO mice using an 8-arm radial maze task.
- To evaluate the efficacy of a combination antioxidant therapy (CAT) in mitigating cognitive deficits in ApoE KO mice.
- To clarify the relationship between ApoE genotype, AD pathology, and cognitive function.
Main Methods:
- Spatial memory assessment in ApoE KO mice and control groups using an 8-arm radial maze.
- Longitudinal comparison of memory performance between strains.
- Administration and evaluation of combination antioxidant therapy (CAT) on memory function.
Main Results:
- ApoE KO mice demonstrated superior reference memory and fewer incorrect entries compared to control mice.
- No significant strain differences were found in working memory errors.
- Combination antioxidant therapy (CAT) did not significantly impact memory performance in either group.
Conclusions:
- ApoE genotype influences spatial memory performance, with ApoE KO mice exhibiting enhanced reference memory.
- The 8-arm radial maze task provides a sensitive measure for spatial memory in AD mouse models.
- Combination antioxidant therapy was ineffective in improving cognitive function in this model of AD.

